As reports filter through that NHS 24 is receiving 50 calls per hour about the remarkable TauRx Therapeutics Ltd trial of Rember™, Scotland must remember the needs of the 62,500 people with dementia for whom a cure may be several years (or more) away.

Jim Jackson, Chief Executive of Alzheimer Scotland, said, “Although this news of a potential cure for Alzheimer’s is extremely encouraging, it will be at least four years (future trial success permitting) before it is available on prescription. The high numbers of calls to our Dementia Helpline and to NHS 24 since these results were made public only further highlight the very real needs of people with Alzheimer’s (and other forms of dementia) right now.

“Our 2008 report Meeting our needs? - the level and quality of dementia support services in Scotland revealed serious deficiencies in the amount and quality of care services available for people with dementia and their carers. It is essential that steps are taken now to relieve the pressure on services and plan for the future increase in the numbers of people with dementia.”

Alzheimer Scotland

Alzheimer’s Society comment: Living with a partner in midlife can reduce your risk of dementia, according to new research presented at the International Conference on Alzheimer’s Disease.

‘Some evidence suggests remaining socially active may reduce your risk of dementia and living with someone is certainly a good way of increasing social interaction. Whether its reaching for the vacuum cleaner or going for long romantic walks, lifestyle factors associated with being married may also help.

However, singletons shouldn’t worry - there are many other ways to reduce your risk of dementia that don’t involve popping the question. The best evidence is around eating a Mediterranean diet, exercising regularly and not smoking.’

Susanne Sorensen
Head of Research
Alzheimer’s Society

Reference

Krister H?kansson. Unmarried life: Paving the way for dementia?

About dementia

- 1 in 3 people over 65 will end their lives with a form of dementia.

- 700,000 people in the UK have a form of dementia, more than half have Alzheimer’s disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051. 1 in 6 people over 80 have dementia.

- The Alzheimer’s Society champions the rights of people living with dementia and those who care for them. The Alzheimer’s Society works in England, Wales and Northern Ireland.

- As a charity, the Alzheimer’s Society depends on the generosity of the public to help it care, research and campaign for people with dementia. You can donate now by calling 0845 306 0898 or visiting http://www.alzheimers.org.uk.

Alzheimer’s Society

Medivation, Inc. (NASDAQ: MDVN) announced new data showing that its investigational drug Dimebon continues to produce broad, clinically meaningful benefits in Alzheimer’s disease patients after long-term dosing, and appears to operate through a novel mechanism of action. These data were presented recently in a podium session and two poster sessions at the 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD) in Chicago. The presentations are highlighted below.

Dimebon Preserves All Key Functions in Alzheimer’s Patients for 18 Months in Open-Label
Extension of First Pivotal Trial

New data from a six-month open-label extension of the 12-month placebo-controlled study of Dimebon in patients with mild-to-moderate Alzheimer’s disease demonstrated that Dimebon continued to improve the clinical course of the disease. After 18 months of treatment, Dimebon preserved function in patients at their original levels upon entering the trial across all key aspects of Alzheimer’s disease, specifically memory and thinking, behavior, activities of daily living and overall function. These results are noteworthy as untreated Alzheimer’s patients progressively deteriorate over time in these areas. Dimebon remained well tolerated throughout the 18-month treatment period.

The open-label extension data were presented in a poster session by Jeffrey Cummings, M.D., Director of the Mary S. Easton Center for Alzheimer’s Disease Research at UCLA. “To my knowledge, no other approved or investigational treatment has stabilized function across all facets of Alzheimer’s disease for this length of time,” said Dr. Cummings. “These data suggest that Dimebon may provide long-term benefits to Alzheimer’s patients and provide further support for its potential as a promising therapeutic to treat this devastating disease.”

Patients originally on placebo for 12 months who were then crossed over to Dimebon in the openlabel extension phase stabilized across all key measures tested. Since these patients had declined over the previous 12 months while on placebo, they generally stabilized at a lower level of function than those treated with Dimebon for the full 18 months, suggesting a benefit of earlier treatment.

Dimebon Benefits Both Mild and Moderate Patients in 12-month Subgroup Analyses

New data from subgroup analyses by disease severity of the Dimebon double-blind placebocontrolled trial showed that Dimebon benefited both mild and moderate patients. In both mild and moderate patients, Dimebon treatment resulted in significant benefit on the study’s primary endpoint, the Alzheimer’s Disease Assessment Scale-cognition subscale, or ADAS-cog. The benefit in the moderate subpopulation was particularly robust, with a 9.7 point drug-placebo difference on the ADAS-cog (p<0.0001) after 12 months of treatment.

The subgroup analyses were presented in a separate poster presentation at ICAD 2008 by Rachelle Doody, M.D., Ph.D., the Effie Marie Cain Chair in Alzheimer’s Disease Research at the Alzheimer’s Disease and Memory Disorders Center, Baylor College of Medicine in Houston. “A nearly 10-point improvement over placebo in moderate patients on the ADAS-cog, a well-validated cognition scale in Alzheimer’s disease, is unquestionably of clinical significance, especially in light of a clinical effect seen on the clinician’s assessment of global function,” said Dr. Doody. “If the results we saw for both the mild and moderate patients can be replicated, I believe that Dimebon will be an important advance in the treatment of Alzheimer’s disease, regardless of stage.”

Dimebon’s Novel Mechanism of Action

In a podium presentation at ICAD 2008, Medivation presented new data on Dimebon’s novel mitochondrial mechanism of action. Mitochondria generate energy for cells and play important roles in mediating cell function and survival. Mitochondrial dysfunction has been linked in the published literature to both Alzheimer’s and Huntington’s diseases. Preclinical data presented showed that Dimebon improves mitochondrial function in the setting of cellular stress with very high potency. For example, Dimebon treatment improved mitochondrial function and increased the number of surviving cells after treatment with a cell toxin known as ionomycin in a dose-dependent fashion. The effect of Dimebon to improve mitochondrial dysfunction has been confirmed in the independent laboratory of Maria Ankarcrona, Ph.D., Associate Professor at the Karolinska Institutet in Sweden.

“All of the approved Alzheimer’s disease drugs operate by one of two mechanisms - cholinesterase inhibition or NMDA-receptor antagonism,” noted Bengt Winblad, M.D., Ph.D., Head of the Karolinska Institutet’s Alzheimer’s Disease Research Center. “The body of preclinical and clinical data generated thus far convinces me that Dimebon is exerting its effects through a different mechanism. The data presented today support the hypothesis that Dimebon improves mitochondrial dysfunction. This is a novel mechanism that may, in part, explain the clinical benefits seen in Alzheimer’s patients treated with Dimebon.”

About the Pivotal Study

Dimebon’s first pivotal Alzheimer’s trial was a randomized, double-blind, placebo-controlled study of 183 patients with mild to moderate Alzheimer’s disease. In this study, patients treated with Dimebon experienced statistically significant improvements compared to placebo in all the key aspects of the disease: memory and thinking, activities of daily living, behavior and overall function - after both six months and a full year of treatment. Dimebon’s benefit over placebo continued to increase throughout the 12-month treatment period. At the end of 12 months, Dimebon-treated patients preserved their starting level of function on each measure of Alzheimer’s disease. Results of the pivotal study were published in the July 19, 2008 issue of The Lancet.

Earlier this year, the U.S. Food and Drug Administration (FDA) informed Medivation that this study can be used as one of the pivotal studies required to support the approval of Dimebon to treat mildto- moderate Alzheimer’s disease, as long as a significant proportion of the sites in the confirmatory Phase 3 trial are located in the United States. The Company recently began a confirmatory pivotal Phase 3 trial of Dimebon in Alzheimer’s disease known as the CONNECTION study. Patients and caregivers can learn more about the study by visiting http://www.connectionstudy.com or by calling 1-877-888-6386.

About the Open-Label Extension

All patients who completed 12-months of dosing in the first pivotal trial were eligible to enroll in an open-label extension. All participants in the open-label extension received Dimebon, including patients who had previously received placebo during the prior 12 months of the trial. Because there was no placebo-control in the open-label extension, direct comparisons versus placebo cannot be made.

About Dimebon

Dimebon is an orally available small molecule that has been shown to inhibit brain cell death in preclinical models relevant to Alzheimer’s and Huntington’s diseases, making it a potential treatment for these and other neurodegenerative diseases. Preclinical data generated to date suggest that Dimebon operates through a novel mitochondrial mechanism of action. On July 7, 2008, Medivation announced positive safety and efficacy results from its Phase 2 trial of Dimebon for the treatment of Huntington’s disease, which was conducted in collaboration with the Huntington Study Group. The study met its primary endpoint of safety and tolerability; in addition, Dimebon showed statistically significant benefit versus placebo in cognition as measured by the Mini-Mental State Examination, a secondary endpoint in the study. Huntington’s disease is a progressive neurodegenerative disease characterized by the gradual development of involuntary muscle movement, progressive deterioration of cognitive processes and memory and severe behavioral disturbances. There are currently no approved drugs in the United States to treat this uniformly fatal genetic disorder.

About Medivation

Medivation, Inc. is a biopharmaceutical company focused on the rapid development of novel small molecule drugs to treat serious diseases for which there are limited treatment options. Medivation aims to transform the treatment of these diseases and offer hope to critically ill patients and their caregivers. The Company’s current clinical development program includes a pivotal and confirmatory Phase 3 trial of Dimebon in Alzheimer’s disease and a Phase 1-2 clinical trial of MDV3100 in patients with castration-resistant (also known as hormone-refractory) prostate cancer. Medivation recently announced that it plans to continue further development of Dimebon in patients with mild-to-moderate Huntington’s disease based on the positive results seen in its Phase 2 trial. For more information, please visit us at http://www.medivation.com.

This press release contains forward-looking statements, including statements regarding future clinical development plans, which are made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995. Forward-looking statements involve risks and uncertainties that could cause actual results to differ significantly from those projected. You are cautioned not to place undue reliance on the forward-looking statements, which speak only as of the date of this release.] None of the Company’s product candidates has been approved for sale, significant additional animal and human testing is required in order to seek marketing approval for any of its product candidates, and Medivation cannot assure you that marketing approval can be obtained for any of its product candidates. Furthermore, as is typically the case at this stage of the regulatory review process, the FDA has not yet performed an in-depth review of Medivation’s preclinical and clinical data, so its views remain subject to change. Medivation’s filings with the Securities and Exchange Commission, including its current report on Form 8-K filed on June 23, 2008, include information about additional factors that could affect the Company’s financial and operating results.

http://www.medivation.com

Memory Pharmaceuticals Corp. (Nasdaq: MEMY) presented preclinical data for MEM 68626, its lead 5-HT6 antagonist drug candidate, at the 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD) in Chicago. The results demonstrate that MEM 68626 is effective in models of cognition that are considered predictive of efficacy in Alzheimer’s disease and mild cognitive impairment (MCI). In addition, the data suggests the potential for once-daily oral dosing with a favorable safety and toxicology profile.

“We are extremely pleased with the data emerging from our proprietary 5- HT6 antagonist program. MEM 68626 produces a robust effect in key models of cognition with a favorable safety and pharmacokinetic profile, providing a strong rationale for clinical development in a cognition indication,” stated Vaughn M. Kailian, President and Chief Executive Officer of Memory Pharmaceuticals. “We look forward to advancing this program into the clinic by year-end.”

The results were presented in a poster titled “Characterization of serotonin 5-HT6 receptor antagonists as putative drugs for age-related mild cognitive impairment and Alzheimer’s disease.” The data included the following:

— MEM 68626 significantly enhanced object recognition in young rats, demonstrating improvements in both acquisition and consolidation memory processes in a model of episodic memory.

— In a model of spatial reference memory, MEM 68626 restored cognitive function in aged-impaired rats, and this effect was maintained with longer- term dosing.

— The data suggests that MEM 68626 was active in the cortical and hippocampal areas of the brain, critical regions that are compromised in Alzheimer’s disease and MCI.

— Pharmacokinetic studies of MEM 68626 demonstrated that the compound achieved plasma and brain exposure levels sufficient for once-a-day dosing.

Memory Pharmaceuticals also presented a poster titled “Working Memory Deficits in rTg4510 Tau Transgenic Mice,” which was selected as a “Hot Topics” presentation.

About MEM 68626

MEM 68626 is a novel, potent and selective antagonist of the 5-HT6 receptor, a validated target for the treatment of cognitive disorders. The compound has demonstrated efficacy in multiple preclinical models of cognition and obesity and has a favorable safety and toxicology profile in animal studies. MEM 68626 is the lead compound in Memory Pharmaceuticals’ 5-HT6 antagonist program.

About the Company

Memory Pharmaceuticals Corp., a biopharmaceutical company, is focused on developing innovative drugs for the treatment of debilitating CNS disorders, many of which exhibit significant impairment of memory and other cognitive functions, including Alzheimer’s disease and schizophrenia. For additional information, please visit our website at http://www.memorypharma.com.

Safe Harbor Statement

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 that are subject to risks and uncertainties. All statements, other than statements of historical facts, regarding management’s expectations, beliefs, goals, plans or Memory Pharmaceuticals’ prospects, future financial position, future revenues and projected costs should be considered forward-looking. Readers are cautioned that actual results may differ materially from projections or estimates due to a variety of important factors, including the outcome of clinical trials of Memory Pharmaceuticals’ drug candidates and whether they demonstrate these candidates’ safety and effectiveness; the risks and uncertainties associated with: obtaining additional financing to support Memory Pharmaceuticals’ R&D and clinical activities and operations; obtaining regulatory approvals to conduct clinical trials and to commercialize Memory Pharmaceuticals’ drug candidates; Memory Pharmaceuticals’ ability to enter into and maintain collaborations with third parties for its drug development programs; Memory Pharmaceuticals’ dependence on its collaborations and its license relationships; achieving milestones under Memory Pharmaceuticals’ collaborations; Memory Pharmaceuticals’ dependence on preclinical and clinical investigators, preclinical and clinical research organizations, manufacturers and consultants; protecting the intellectual property developed by or licensed to Memory Pharmaceuticals; and Memory Pharmaceuticals’ ability to maintain listing on the Nasdaq Global Market. These and other risks are described in greater detail in Memory Pharmaceuticals’ filings with the Securities and Exchange Commission. Memory Pharmaceuticals may not actually achieve the goals or plans described in its forward-looking statements, and investors should not place undue reliance on these statements. Memory Pharmaceuticals disclaims any intent or obligation to update any forward-looking statements as a result of developments occurring after the date of this press release.

Memory Pharmaceuticals Corp.
http://www.memorypharma.com

A new study suggests that those who are unmarried or not living with a partner in midlife could have an increased risk of developing Alzheimer’s disease, according to research reported today at the 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008), in Chicago.

Additional research on Alzheimer risk factors presented at ICAD 2008 indicates that people who ruminate, or repeatedly think about their problems, may be less likely to develop the disease, while people with metabolic syndrome (a combination of cardiovascular health related symptoms) are at higher risk. Finally, a large meta-analysis of nine European risk factor surveys confirmed a well recognized group of Alzheimer risk factors, including memory complaint, severe head trauma, diabetes, stroke and low education.

“We may not be able to do anything about aging, genetics or family history, but research shows us that there are lifestyle decisions we all can make to keep our brains healthier as we age, and that also may lower our risk of developing Alzheimer’s disease,” said William Thies, PhD, vice president for Medical & Scientific Relations at the Alzheimer’s Association.

Unmarried Life: Paving the Way for Dementia?

Research suggests that maintaining regular social interaction can contribute to maintaining brain health as we age and possibly decrease one’s risk of developing Alzheimer’s. When people are married they are able to have close interaction on a regular basis. This may reduce the occurrence of dementia.

Krister Hakansson, BA, of Karolinska Institutet, KI Alzheimer Research Center, Stockholm, Sweden and Vaxjo University, School of Social Sciences, Vaxjo, Sweden, conducted a first-of-its-kind evaluation of whether midlife marital status is related to late-life cognitive function. The study examined 1,449 individuals from the Finnish Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study in midlife and then again in 1998, an average of 21 years later.

At re-examination, 139 persons were diagnosed with some form of cognitive impairment: 82 with mild cognitive impairment (MCI) and 48 with Alzheimer’s. Persons in the study who were living with a partner in midlife were significantly less likely to show cognitive impairment compared to all other categories (single, separated, divorced or widowed). Those in the study who were married or lived with a significant other in midlife had a 50% lower risk of having dementia in late-life compared to those who lived alone, even after adjustments for education, BMI, cholesterol, blood pressure, occupation, physical activity, smoking habits, depression, ApoE status, age at follow-up and gender.

The researcher observed that there were differences between groups of people who had been living alone for different reasons. The all-life singles had a doubled risk, whereas the ones who stayed divorced from midlife onwards had a tripled risk. The most dramatic risk increase was found for those widowed before midlife and who stayed widowed. Compared to those married at midlife and still so at late-life, they had more than a six-fold risk of developing Alzheimer’s.

“Living in a couple relationship is normally one of the most intense forms of social and intellectual stimulation. If social and cognitive challenges can protect against dementia, so should living in a couple relation,” said Hakansson. “This study points to the beneficial effects of a married life, consistent with the general hypothesis of social stimulation as a protective factor against dementia.”

Tendency for Rumination in Midlife May Decrease Risk for Dementia Decades Later

According to Ramit Ravona-Springer, MD, of Sheba Medical Center, Tel Hashomer, Ramat Gan, Israel and colleagues, “rumination” refers to the disposition for repetitive thinking over one’s problems.

Tendency for rumination when confronting difficulties in family and work settings was assessed in about 9,000 participants in the IIHD study, a longitudinal investigation of the incidence and risk factors for cardiovascular disease among Jewish male civil servants in Israel. Tendency for rumination was assessed as 1=always forget, 2=tend to forget, 3=tend to ruminate, 4=usually ruminate.

Dementia was assessed three decades later in 1,890 participants among 2,604 survivors of the original cohort. Mean age of the participants was 82 at the time of final assessment. 308 were diagnosed as demented, 175 as having mild cognitive impairment, and 1,407 had no cognitive impairment.

The prevalence rates of dementia (adjusted for age, area of birth, and socioeconomic status) were 21% for those who always forget difficulties in familial settings, 18% for those who tend to forget, 14% for those who tend to ruminate over difficulties, and 14% for those who usually ruminate. When rumination in response to difficulties at work was assessed, prevalence rates of dementia were 24% for those who always forget difficulties, 19% for those who tend to forget, 15% for those who tend to ruminate over difficulties, and 15% for those who usually ruminate.

A total score for rumination in both family and work settings was calculated, and subjects were divided into four groups according to this score. Relative to the group with the lowest total rumination score, dementia prevalence was 30 to 40 percent less in groups with higher scores.

“Your personality traits, specifically your psychological and cognitive style when confronting distress, may be associated with your risk for dementia,” said Ravona-Springer. “However, exactly how this works still needs to be determined.”

Metabolic Syndrome May Lead to Cognitive Decline

Metabolic syndrome (Met.S) is a group of heart disease risk factors that includes abdominal obesity, elevated blood pressure, high triglycerides, elevated blood sugar and low HDL cholesterol. Those who have Met.S are at higher risk for developing diabetes, hypertension, and stroke, all of which increase the risk of developing dementia, including Alzheimer’s disease.

Matheus Roriz-Cruz, MD, PhD, Federal University of Rio Grande do Sul State, Brazil and colleagues studied the effects of Met.S on the development of cognitive impairment in people who have not had a stroke. Researchers evaluated 422 healthy elderly men and women over age 60 in Brazil and used a battery of scales to assess cognition, depression, planning and activities of daily living. Met.S was present in 39.3% of participants.

Data from the study revealed that all neurofunctional scores were significantly lower for those with Met.S, and the difference increased with age. Older people with Met.S had an almost 35% higher level of cognitive compromise when compared to those without Met.S.

“Met.S was independently associated with lower cognitive, planning, neuromotor and functional scores, and with more depressive symptoms,” said Roriz-Cruz. “The results from this study reinforce the importance of maintaining good physical health in order to reduce one’s risk of experiencing cognitive decline, and possibly developing Alzheimer’s disease.”

Risk Factors for Progression to Dementia in General Population

In the general population, many risk factors and predictors for dementia have been identified. However, a combination of risk factors may give a more accurate prediction for dementia than each individual risk factor.

Sylvaine Artero, of INSERM, Montpellier, France; Pieter Jelle Visser, of the University of Maastricht, The Netherlands; and colleagues analyzed a pooled database constructed from nine European surveys of dementia risk factors, including a total of 16,261 participants over age 55 without dementia. Potential risk factors were evaluated at baseline and incident dementia was assessed over a follow up period of up to 15 years. Risk factors included cardiovascular disorders, endocrine disorders, depression, head trauma, intoxicants (including alcohol, smoking and drugs), physical and intellectual activities, performance in activities of daily living, Apolipoprotein E genotype, cognitive complaint, and cognitive test performance.

In total, 1,530 subjects (9%) progressed towards dementia. In order, the most predictive variables were: impairment in executive function (planning), memory problems (as measured on tests), subjective complaints about memory/cognitive failure, Apolipoprotein E (ApoE) genotype, use of psychotropic medication, severe head trauma, diabetes, stroke, and problems with language. In addition, problems with activities of daily living, smoking, no drinking, no use of hypertensive drugs, low education, and female gender all independently predicted dementia at follow-up.

“Cases of dementia in the general population can be best identified by a combination of socio-demographic, clinical and cognitive factors,” said Artero. “Developing a better understanding of the factors that increase risk for Alzheimer’s will help us to create more effective methods to prevent people from developing the disease.”

About ICAD 2008

The 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008) is the largest gathering of international leaders in Alzheimer research and care ever convened. At ICAD 2008, more than 5,000 researchers from 60 countries will share groundbreaking information and resources on the cause, diagnosis, treatment and prevention of Alzheimer’s and related disorders. As a part of the Association’s research program, ICAD serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community. ICAD 2008 will be held in Chicago at McCormick Place, Lake Side Center from July 26-31.

About the Alzheimer’s Association

The Alzheimer’s Association is the leading voluntary health organization in Alzheimer’s research, care and support. Our mission is to eliminate Alzheimer’s disease through the advancement of research, provide and enhance care and support for all affected, and reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer’s. For more information, visit http://www.alz.org.

— Krister Hakansson - “Unmarried life: Paving the way for dementia?” (Funders: Gun and Bertil Stohne Foundation)

— Ramit Ravona-Springer - “Tendency for rumination as a psychological cognitive style in midlife is associated with decreased risk for dementia three decades later.” (Funders: Israel Science Foundation, Israel Academy of Sciences and Humanities)

— Matheus Roriz-Cruz - “Metabolic syndrome, successful and pathological neuroaging in a stroke-free elderly population.” (Funders: Ministries of Education, Brazil and Japan)

— Sylvaine Artero, Pieter Jelle Visser - “Risk factors for progression to dementia in general population: the Descripa study (European pooled data base).” (Funder: European Commission, 5th framework programme (QLK-6-CT-2002-02455))

Alzheimer’s Association
http://www.alz.org

Results from clinical trials of three potential Alzheimer’s therapies raise hope for new and better treatments of the disease, according to data reported today at the 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008) in Chicago.

A related study showed that taking antidementia drugs appears to have a positive impact on extending lifespan in those with Alzheimer’s.

These reports included:

Eighteen-month data from an open-label extension of a pivotal trial of Dimebon (Medivation) in mild to moderate Alzheimer’s.

— Nine-month data from an interim analysis of the first U.S. Phase II trial of intravenous immunoglobulin, or IVIg (Baxter), in Alzheimer’s.

— Results of a Phase II study of a monoclonal antibody (LY2062430, Lilly) in mild to moderate Alzheimer’s.

— Research suggesting that persistent antidementia drug use increases survival in people with Alzheimer’s.

“Therapies targeting amyloid in Alzheimer’s disease must continue to be thoroughly tested,” said William Thies, PhD, Alzheimer’s Association vice president for Medical and Scientific Relations. “At the same time, we know that Alzheimer’s is a complex disease and that better treatments and preventions will likely also be complex, so we must investigate every promising drug target looking eventually towards the possibility of a multi-strategy approach.”

18-Month Data from an Extension of a Pivotal Trial of Dimebon in Alzheimer’s

In a study recently reported, Dimebon (Medivation) improved cognition and memory, activities of daily living, and behavior in a one-year placebo-controlled trial of patients with mild to moderate Alzheimer’s. At ICAD 2008, Jeffrey L. Cummings, M.D., the Augustus S. Rose Professor of Neurology, and Professor of Psychiatry and Biobehavioral Sciences, at UCLA, and colleagues reported on an open-label extension of the trial to 18 months.

One hundred eighty-three (183) people with mild-to-moderate Alzheimer’s were initially randomized into a six-month placebo-controlled study of Dimebon. Patients completing six months of treatment were offered the opportunity to re-consent for an additional six months of controlled treatment in their originally randomized group, followed by an open-label extension (OLE). Data presented at ICAD 2008 include only the 104 OLE participants (54 Dimebon, 50 placebo). All were given Dimebon for the OLE, not placebo, at a dose of 20 mg three times per day. Ninety-two (92) (88.5%) patients enrolling into OLE completed six months of treatment.

Patients originally receiving Dimebon for 12 months who continued on Dimebon for an additional six months in the OLE phase had preservation of function close to their starting baselines on the key signs and symptoms of Alzheimer’s disease 18 months after starting the study. Patients originally on placebo for 12 months who were then crossed over to Dimebon on the OLE phase also stabilized across all key measures tested. Since these patients had declined over the previous 12 months while on placebo, they stabilized at a lower level of function than those treated with Dimebon for the full 18 months.

Dimebon was well-tolerated through 18 months. Adverse events that occurred more often with dimebon compared to placebo were dry mouth, sweating and depressed mood/sadness.

“People initially treated with placebo and then crossed over to Dimebon did not show the same level of benefit as those people who took Dimebon for the full 18 months,” Cummings said. “This emphasizes the benefit of earlier treatment, and suggests the possibility that Dimebon may slow of the progression of Alzheimer’s. However, open-label extensions are not that same as placebo-controlled trials, and extrapolation of the treatment results should be done with caution. Patients are being screened now for the Phase III clinical trials.”

“Dimebon appears to work through a mechanism of action that is distinct from currently marketed Alzheimer’s drugs. Dimebon improves impaired mitochondrial function. Mitochondria are the central energy source of all cells and impaired mitochondrial function may play a significant role in the loss of brain cell function in Alzheimer’s,” Cummings added.

First U.S. Double-Blind Phase II Clinical Trial of IVIg (Immunotherapy) in Alzheimer’s

IVIg is under investigation by Baxter International as a potential anti-amyloid immunotherapy for Alzheimer’s. It contains a broad spectrum of antibodies, and is currently indicated as a therapy for people with primary immunodeficiency disorders. IVIg contains antibodies that bind to the beta amyloid aggregates that are thought to be central to Alzheimer’s. In two previous open-label studies, patients with mild to moderate Alzheimer’s showed cognitive improvement when treated with IVIg for six months.

Diamanto Tsakanikas, PhD, Norman Relkin, MD, PhD, and colleagues at Weill Cornell Medical College carried out a six-month Phase II double-blind, placebo-controlled study of IVIg for Alzheimer’s followed by a 12-month, rater-blinded extension study. At ICAD 2008, they reported an interim analysis of uninterrupted IVIg treatment for 9 months.

Twenty-four people with mild to moderate Alzheimer’s (MMSE 14-26) participated in the trial. For the first six months, eight participants received placebo and 16 received IVIg at four doses ranging from 0.2 grams IVIg per kilogram of body weight every two weeks to 0.8 grams IVIg per kilogram of body weight given once per month (four people each at the four different doses). After six months, all subjects were given IVIg with the raters blinded to dose. The primary outcome measures were two standard measures of cognition and the clinician’s observation of change (a seven point scale from “markedly improved”=+3 to “marked worsening”=-3), respectively the ADAS-cog and the ADCS-CGIC, which were administered at baseline and three-month intervals thereafter.

In the total group, the researchers found statistically significant differences favoring IVIg treatment on the CGIC at three, six and nine months. At nine months, the IVIg group averaged 1.5 points higher on the CGIC. On the ADAS-cog, scores favoring IVIg reached statistical significance at nine months. The average change in ADAS-Cog score at nine months favored IVIg treatment by 5.4 ADAS points. Uninterrupted IVIg treatment also produced sustained benefits relative to initial placebo treatment in activities of daily living.

When the results for each dose were analyzed individually, subjects receiving 0.4 grams of IVIg per kilogram of body weight given every two weeks improved over baseline on ADAS-Cog, ADCS-CGIC, and a measure of daily functioning. The researchers identified this as the best dose. None of the subjects given placebo showed comparable improvements.

Treatment-related adverse events that occurred at a greater frequency with IVIg treatment as compared to placebo were rash and a transient drop in blood count. In contrast, there were more behavioral disturbances in placebo-treated patients than those who received IVIg.

“While there were relatively small numbers of participants in this study, we were nonetheless able to demonstrate that people with Alzheimer’s who get uninterrupted treatment with IVIg for nine months have statistically significant and clinically relevant improvements on both cognitive and global clinical measures,” Tsakanikas said. “A large-scale, 18-month, multicenter Phase III clinical trial of IVIg in Alzheimer’s is now getting underway, sponsored by Baxter and the National Institutes of Health, that will test whether IVIg immunotherapy provides long-term benefits and has a disease-modifying effect. Additional studies may be required.”

Phase II Immunotherapy Trial with LY2062430 in Mild to Moderate Alzheimer’s

Previous research has shown that antibodies that bind to beta amyloid can be given intravenously. By binding to beta amyloid and increasing the rate of its removal from the body, these antibody infusions may slow the progression of Alzheimer’s.

Eric Siemers, MD, Medical Director of the Alzheimer’s Disease Research Team at Eli Lilly and Company, and colleagues conducted a Phase II trial of a monoclonal antibody, known as LY2062430, that binds to the mid-domain of beta amyloid.

Fifty-two (52) people with mild to moderate Alzheimer’s and 16 volunteer subjects were studied. Alzheimer’s patients received 12 weekly infusions of placebo or antibody (100 mg every 4 weeks, 100 mg once per week, 400 mg every 4 weeks or 400 mg once per week). Volunteers received a single 100 mg dose of antibody. Safety assessments included brain imaging using magnetic resonance imaging (MRI) and examination of cerebrospinal fluid (CSF, a fluid normally present around the brain and spinal cord). In an optional sub-study, 24 Alzheimer’s patients and 13 volunteers underwent a type of brain imaging known as SPECT using a tracer (known as IMPY) that measures the amount of amyloid plaque present in the brain. Measures of symptom severity were obtained in all AD patients using the Alzheimer’s Disease Assessment Scale - Cognition (ADAS-cog).

The researchers found that following administration of the antibody, the amount of beta amyloid in blood increased substantially after the antibody bound to the beta amyloid protein. A small amount of the antibody enters the CSF, and in the Alzheimer’s patients beta amyloid also increased in CSF, similarly bound to the antibody. For patients treated with 400 mg of the antibody, the amount of the type of beta amyloid primarily found in plaque (known as AB1-42) that appeared in the blood correlated with the amount of amyloid plaque in the brains based on IMPY scans (r=0.65, p=0.02). According to Siemers, this finding suggests that some of the beta amyloid protein present in plaque moves to blood after treatment with the antibody.

Certain other types of beta amyloid thought to be primarily or exclusively found in amyloid plaque are also increased in blood and CSF of study participants. The antibody produced no change in cognitive scores or in the total amount of amyloid plaque based on IMPY scans. Siemers said that this was expected in a study of this duration.

According to the researchers, brain imaging using MRI and CSF safety assessments showed no evidence of inflammation, bleeding or other side effects throughout the trial. No side effects were identified that appeared to be related to antibody treatment.

“We saw an increase in amyloid beta, which is thought to be bound to LY2062430, in both the blood and cerebrospinal fluid of study participants,” Siemers said. “Additionally, after treatment we found a correlation between beta amyloid in blood and the amount of amyloid plaque in brain as determined by IMPY imaging, as well as an increase in blood and CSF in certain types of beta amyloid found in plaques. These biomarker data suggest that amyloid plaques in the brain may begin to ‘dissolve’ after 12 weeks of treatment with this antibody. We’re now planning a Phase III clinical trial of this drug to be started in 2009.”

Antidementia Drugs Contribute to Longer Life in People with Alzheimer’s

Survival (life span) in people with Alzheimer’s is recognized to be shorter than what is expected in cognitively normal seniors and is recognized to be influenced by several factors including age, disease severity, general debility, and gender. Approved antidementia drugs have been shown help with the symptoms of Alzheimer’s but their influence on life span is not known.

At ICAD 2008, Susan Rountree, MD, of the Alzheimer’s Disease and Memory Disorders Center of Baylor College of Medicine in Houston, Texas, reported on a study of the persistent use of antidementia drugs and their influence on survival.

The researchers followed 641 people diagnosed with Alzheimer’s at an academic medical clinic between 1989 and 2007. These individuals had been on drug therapy over the course of their Alzheimer’s for variable amounts of time and the majority had used one or more of the commercially available antidementia drugs (donepezil, galantamine, rivastigmine, tacrine, or memantine).

Total years on medication was divided by the total years of disease symptoms to determine a persistency score for each individual. Participants were divided into four groups (1st, 2nd, 3rd, 4th quartiles) ranging from the lowest to highest persistency scores and the researchers compared life span among the groups after adjustment for a variety of factors generally recognized to influence survival. The 1st quartile took drug less than 33 percent of the time, 2nd quartile = 34-55 percent of the time, 3rd quartile = 56-70 percent of the time, and the 4th quartile = 71-99 percent of the time.

Over the entire course of the study, 12 percent of participants never took any antidementia drugs. Fifty-three (53) percent of the participants died.

The researchers found an inverse and statistically significant relationship between the overall risk of death and the persistency of drug use. Those in the lowest persistency group (1st quartile) were 2.4 times more likely to die than those in the highest persistency group (4th quartile). Those with intermediate drug exposure had increased risk of death of 2.2 times (2nd quartile) and 1.5 times (3rd quartile) compared to the most persistent users. More persistent therapy was associated with a longer median survival time; the median survival between the lowest quartile group and the most persistent users was 3.12 years.

“In our study, people with Alzheimer’s who took antidementia drugs more persistently lived longer than those who took the medications for shorter time intervals,” Rountree said. “In an earlier study involving this group, we reported that persistency of treatment was also associated with long term cognitive and functional benefits. Persistent drug therapy appears to help Alzheimer’s patients live longer and the mechanism may be related to overall improvement of cognition and function resulting from current symptomatic therapies.”

About ICAD 2008

The 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008) is the largest gathering of international leaders in Alzheimer research and care ever convened. At ICAD 2008, more than 5,000 researchers from 60 countries will share groundbreaking information and resources on the cause, diagnosis, treatment and prevention of Alzheimer’s and related disorders. As a part of the Association’s research program, ICAD serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community. ICAD 2008 will be held in Chicago at McCormick Place, Lake Side Center from July 26-31.

About the Alzheimer’s Association

The Alzheimer’s Association is the leading voluntary health organization in Alzheimer’s research, care and support. Our mission is to eliminate Alzheimer’s disease through the advancement of research, provide and enhance care and support for all affected, and reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer’s. For more information, visit http://www.alz.org.

— Jeffrey Cummings. “18-Month data from an open-label extension of a one-year controlled trial of dimebon in patient with mild-to-moderate Alzheimer’s disease.” (Funder: Medivation)

— Diamanto Tsakanikas. - “Effects of uninterrupted intravenous immunoglobulin treatment of Alzheimer’s disease for 9 months.” (Funder: Baxter International)

— Eric R. Siemers. - “Safety, tolerability and biomarker effects of an Abeta monoclonal antibody administered to patients with Alzheimer’s disease.” (Funder: Eli Lilly and Company)

— Susan Rountree. - “Persistent Antidementia Drug Treatment and Survival in an Alzheimer’s Disease Cohort.” (Funders: Forest Research Institute and The Cynthia and George Mitchell Foundation)

All materials to be presented at the 2008 Alzheimer’s Association International Conference on Alzheimer’s Disease (ICAD 2008) are embargoed for publication and broadcast until the date and time of presentation at the International Conference on Alzheimer’s Disease, unless the Alzheimer’s Association provides written notice of change of date/time in advance.

Alzheimer’s Association
http://www.alz.org

Eli Lilly and Company (NYSE: LLY) announced interim results of its Phase II study of LY2062430, an investigational anti-amyloid beta monoclonal antibody for the treatment of mild to moderate Alzheimer’s disease. In this study, intravenously administered LY2062430 bound to the amyloid beta protein, resulting in increased amounts of amyloid beta in participants’ blood and cerebrospinal fluid. These and other results suggest that by binding to soluble amyloid beta proteins, LY2062430 may begin to dissolve the amyloid plaques that are present in the brains of patients with Alzheimer’s disease. While the precise cause of Alzheimer’s disease is not known, it has been shown that people with this disorder have an excess of amyloid beta plaque in the brain, particularly in the regions associated with memory. It is theorized that decreasing the total amount of amyloid plaque and other forms of the amyloid beta protein in the brain may result in slowing of the disease progression. Importantly, LY2062430 was well tolerated with no evidence of treatment-related brain inflammation, bleeding or other side effects. The findings from this Phase II study were presented today at the Alzheimer’s Association’s 2008 International Conference on Alzheimer’s Disease (ICAD) in Chicago.

In this randomized, controlled trial, researchers evaluated the safety and tolerability of LY2062430 administered intravenously in patients with Alzheimer’s disease and in healthy volunteers. They assessed the effects of the antibody on levels of amyloid beta in the blood and cerebrospinal fluid, as an indirect measure of the effect of the antibody on amyloid beta present in the brain. Cerebrospinal fluid, which surrounds the brain and spinal cord, is thought to provide important biomarker data in addition to that obtained from blood. Amyloid plaques, the pathological hallmark of Alzheimer’s disease, are composed largely of aggregated amyloid betaproteins. Amyloid plaques or other types of the amyloid beta protein are thought ultimately to disrupt normal nerve cell function in the brain, leading to the dementia that characterizes Alzheimer’s disease.

“We are encouraged that in this study, we saw increased amyloid beta which is thought to be bound to LY2062430, in both the blood and cerebrospinal fluid. We hypothesize that this effect may lead to reduced formation of amyloid plaques in the brain after long-term treatment,” said Eric Siemers, M.D., Medical Director, Alzheimer’s disease research for Eli Lilly and Company. “Alzheimer’s disease is complex, and there’s a real need for new treatments that might be shown ultimately to slow disease progression. In addition to the biomarker results, we are particularly encouraged by the finding that patients who received the monoclonal antibody treatment over 12 weeks appeared to have no treatment-related side effects.”

In this 12-week Phase II study, researchers gave 52 mild to moderate Alzheimer’s disease patients infusions of placebo or LY2062430 in varying doses: 100mg or 400mg once a week, or 100mg or 400mg every four weeks. Alzheimer’s disease symptom severity was also evaluated. In addition, 16 volunteers each received a single dose of 100mg of LY2062430 or placebo. For all study participants, safety assessments included magnetic resonance imaging (MRI) and cerebrospinal fluid examinations. A sub-study of 24 patients and 13 volunteers underwent single photon emission tomography (SPECT) scanning using an experimental tracer to assess levels of amyloid beta plaque in the brain.

The interim analysis showed that weekly infusions of LY2062430 up to 400mg per dose was well tolerated, with no side effects related to treatment. An evaluation of MRI brain imaging and an assessment of cerebrospinal fluid showed no evidence of brain inflammation or bleeding. As expected for a study of this duration, no change in patients’ cognitive scores was observed and there was no change in levels of brain amyloid beta plaque as measured by the SPECT tracer. In addition to the increase in the two major forms of the amyloid beta protein seen in blood and cerebrospinal fluid, an increase in the two other types of the amyloid beta protein thought to be present only in amyloid plaques was observed in participants’ blood and cerebrospinal fluid. The biomarker effects lasted for several weeks. These biomarker findings suggest that longer term treatment with LY2062430 may slow the clinical progression of Alzheimer’s disease, thus providing a rationale for additional trials of LY2062430.

“Results from this Phase II study are promising, and we are pleased to announce our intention to commence a Phase III pivotal study of LY2062430 beginning in 2009,” said Steven M. Paul, M.D., Executive Vice President, Science and Technology, President of Lilly Research Laboratories. “Additionally we are currently enrolling patients into the Phase III study called IDENTITY, which examines treatment with LY450139, an investigational gamma secretase inhibitor believed to slow the rate of formation of amyloid beta, potentially slowing disease progression. These two neuroscience pipeline candidates represent potentially important advances in the effort to slow the progression of this fatal disease, and demonstrate our longstanding commitment to developing treatments for devastating brain illnesses.”

About Alzheimer’s Disease

Alzheimer’s disease is a progressive neurodegenerative condition that is the most common cause of dementia in patients over 65 years of age. Estimates show that 6-8 percent of people older than age 65 are affected by Alzheimer’s disease(1), totaling approximately 5 million people in the United States alone(2). Every 72 seconds, an American is developing Alzheimer’s disease(3), and it is the seventh-leading cause of death in the United States(4). The direct and indirect health care costs associated with Alzheimer’s disease in the U.S. are estimated to be about $150 billion(5). In 2007, the total cost worldwide was estimated at $315.4 billion(6).

Given the aging population, without the availability of medicines that delay or prevent the onset of Alzheimer’s disease, the number of affected people worldwide is expected to quadruple by the year 2050(7). The average duration between onset of symptoms and death due to complications of Alzheimer’s disease is about 8-10 years(8). The burden to caregivers and health care costs can increase dramatically in the late stages of Alzheimer’s disease, when patients cannot maintain independent function and are frequently bedridden.

About LY2062430

LY2062430 binds specifically to soluble amyloid beta and thereby alters the sticky characteristics of this peptide. Alzheimer’s disease theory suggests that amyloid beta kills brain cells. Clinical studies have examined the ability of LY2062430 to impact amyloid beta in blood and cerebrospinal fluid and found significant dose-dependent changes. To date, the most frequently occurring side effect experienced in clinical studies with LY2062430 has been mild chills consistent with an infusion reaction. For a more complete listing of potential side effects, prospective clinical trial participants should refer to the informed consent document.

About Lilly

Lilly, a leading innovation-driven corporation, is developing a growing portfolio of first-in-class and best-in-class pharmaceutical products by applying the latest research from its own worldwide laboratories and from collaborations with eminent scientific organizations. Headquartered in Indianapolis, Ind., Lilly provides answers — through medicines and information — for some of the world’s most urgent medical needs. Additional information about Lilly is available at http://www.lilly.com

P-LLY

This press release contains forward-looking statements about the potential of the investigational compound LY2062430 and reflects Lilly’s current beliefs. However, as with any pharmaceutical product under development, there are substantial risks and uncertainties in the process of development and regulatory review. There is no guarantee that the product will receive regulatory approvals, or that the regulatory approval will be for the indication(s) anticipated by the company. There is also no guarantee that the product will prove to be commercially successful. For further discussion of these and other risks and uncertainties, see Lilly’s filing with the United States Securities and Exchange Commission. Lilly undertakes no duty to update forward-looking statements.

References

(1) Small, GW, Rabins, PV, Barry, PP, Buckholtz, NS, DeKosky, ST, Ferris, SH, Finkel, SI, Gwyther, LP, Khachaturian, ZS, Lebowitz, BD, McRae, TD, Morris, JC, Oakley, F, Schneider, LS, Streim, JE, Sunderland, T, Teri, LA, Tune LE. Diagnosis and Treatment of Alzheimer Disease and Related Disorders: Consensus Statement of the American Association for Geriatric Psychiatry, the Alzheimer’s Association, and the American Geriatrics Society. JAMA 1997; 278: 1363-1371.

(2) Alzheimer’s Association. “2008 Alzheimer’s Disease Facts andFigures.”

(3) American Public Health Association. “Mind Your Memory & Alzheimer’sDisease!”

(4) Centers for Disease Control and Prevention. “National VitalStatistics Reports.”

(5) Alzheimer’s Association. “2008 Alzheimer’s Disease Facts andFigures.”

(6) Wimoa, Anders, Bengt Winblada, and Linus J. Jonssonb. An estimateof the total worldwide societal costs of dementia in 2007. Alzheimer’s &Dementia (2007) 3: 81-91.

(7) Brookmeyer R, Johnson E, Ziegler-Graham K, Arrighi M. Forecastingthe Global Burden of Alzheimer’s disease. Alzheimer’s & Dementia (2007)3:186-191.

(8) National Institute on Aging. “Alzheimer’s Disease Fact Sheet.”Available at http://www.nia.nih.gov/Alzheimers/Publications/adfact.htm.Accessed July 1, 2008.

Eli Lilly and Company
http://www.lilly.com

An overwhelming number of Americans with memory concerns fail to report this health issue with their doctors despite visits within the past six months, according to results released today of a survey of participants in the Alzheimer’s Foundation of America (AFA) National Memory Screening Day last November.

AFA announced the results at a poster session at the Alzheimer’s Association’s 11th International Conference on Alzheimer’s Disease in Chicago.

“The results highlight a significant hole in our healthcare system,” said Eric J. Hall, AFA’s president and chief executive officer. “They re-confirm our fears that this issue is being swept under the carpet and not being talked about with professionals. An open dialogue is essential to proper diagnosis and treatment.”

Richard E. Powers, M.D., chairman of AFA’s Medical Advisory Board, said he is particularly concerned because the aging population is at increased risk of memory issues.

“Not all memory complaints mark Alzheimer’s disease, but if they do, the earlier an individual knows, the earlier he or she can be treated, plan for the future and embrace social services support. This is a window of opportunity to delay cognitive decline and thereby improve quality of life for individuals with the disease and their families,” he said.

The survey involved 2,178 adults who took advantage of free confidential memory screenings at community sites nationwide as part of AFA’s National Memory Screening Day on November 13, 2007, an annual initiative aimed at promoting proper detection of memory concerns, including Alzheimer’s disease and related dementia, and providing education about memory issues and successful aging.

Of the respondents, 68.1 percent self-reported memory complaints, but only 21.1 percent had discussed them with their healthcare providers. This failure to communicate occurred despite recent visits to their primary care physician; of those with memory concerns, 40.3 percent had seen their primary care physician within the last month, and 44.3 percent had an appointment within the last six months.

Failure to report memory symptoms to the respondent’s physician was independent of gender, age, ethnicity or educational background.

In addition, 21 percent said they kept the concerns entirely to themselves. Those who shared their complaints did so with a spouse (41.2 percent), friend (30 percent) or adult child (25.5 percent).

The median age of respondents was 72. While age poses the greatest risk for Alzheimer’s disease, affecting mostly people aged 65 and older, the survey also found that those who came in for screenings had other healthcare concerns that are known risk factors for the brain disorder. Among them, 18.3 percent reported that they are depressed; 16.4 percent have diabetes; and 14.4 percent said they are obese.

“Americans need to step up their efforts to optimize overall health, including brain health. The threat of Alzheimer’s disease and co-existing conditions is too great to ignore,” Powers emphasized.

Asked why participants came in for a screening, 32.3 percent said they were forgetful and 40.6 percent wanted to establish a baseline.

Currently, AFA is gearing up for its 6th annual National Memory Screening Day, which will be held on November 18. Free confidential screenings will be available nationwide at various community sites, including the entire chain of 1,100 Kmart pharmacies, local Alzheimer’s agencies, senior and community centers, assisted living facilities, adult day centers, and doctor’s offices. For information, visit http://www.nationalmemoryscreening.org.

The event is the focal point of AFA’s year-round advocacy efforts to promote proper diagnosis and treatment of Alzheimer’s disease and related dementias, and successful aging. It is overseen by AFA’s Memory Screening Advisory Board, composed of top experts and chaired by John Wesson Ashford, Jr., M.D., senior research scientist at the Stanford/VA Aging Clinical Research Center, Palo Alto, CA.

AFA urges anyone concerned about changes in their memory or other mental functions to visit a local screening site. Warning signs include: forgetting people’s names and events, asking repetitive questions, loss of verbal or written skills, confusion over daily routines, and erratic mood swings.

The face-to-face screening takes about five to ten minutes to complete and consists of a series of simple questions and tasks. It is administered by a qualified healthcare professional, such as a physician, nurse, psychologist, pharmacist, or social worker. It is not a diagnosis, and healthcare professionals encourage those with abnormal scores as well as those who still have concerns to pursue a full medical exam. Follow up with a primary care physician or other clinician may reveal that the person is suffering from a reversible condition such as a vitamin deficiency or thyroid problem, or from an irreversible disorder like Alzheimer’s disease.

The Alzheimer’s Foundation of America is a national nonprofit organization headquartered in New York and made up of more than 950 member organizations that provide hands-on programs to meet the educational, emotional, practical and social needs of families affected by Alzheimer’s disease and related illnesses. AFA’s services include a toll-free hot line, counseling, educational materials, a free caregiver magazine, and professional training.

Alzheimer’s Foundation of America
http://www.alzfdn.org

Medical College of Wisconsin researchers in Milwaukee have reported that children of Alzheimer’s patients who are carriers of a genetic risk factor for Alzheimer’s disease have neurological changes that are detectable long before clinical symptoms may appear.

Functional MRI brain imaging revealed that these symptomless carriers of the APOE-4 gene demonstrated significantly reduced functional brain connectivity between the hippocampus and the posterior cingulated cortex, two important brain structures for memory processing. These structures are relevant for information acquisition, filtering and sorting.

The study, conducted at Froedtert Hospital, was led by Shi Jiang Li, Ph.D., professor of biophysics, and was presented at the Alzheimer’s Association International Conference on Alzheimer’s disease in Chicago, July 29th

“Just as if cancer could be detected when there were only a few cells, decades before it was evident, the advantage of identifying those at great risk for having Alzheimer’s would be of tremendous value in development of interventional therapies,” says Dr. Li.

The researchers studied 28 neurologically-normal subjects, between ages 45 and 65. Twelve carried the APOE-4 gene and 16 did not. The two groups showed no significant difference in age, educational level, or neuropsychological performances. All subjects received fMRI scans. For each subject, functional connectivity between the two brain structures was measured in a resting state.

Results showed that functional connectivity in the non APOE-4 carriers was approximately 65 percent better than that of the carriers.

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Other members of the research team were Piero Antuono, M.D., professor of neurology, and Zhilin Wu, Ph.D., Chunming Xie, Ph.D., and Jennifer L. Jones, M.S., research associates in the departments of biophysics and neurology.

Source: Toranj Marphetia
Medical College of Wisconsin

Alzheimer Scotland welcomes the results of this Phase 2 study on a new treatment for dementia.

Jim Jackson, Chief Executive at Alzheimer Scotland, said, “The initial results of this trial are exciting: responses are extremely encouraging compared to existing treatments. Effectively targeting the protein tangles that kill brain cells would be a new breakthrough in drugs aimed at improving cognition in people with dementia. Alzheimer Scotland looks forward to the academic publication of the Phase 2 study findings in detail and to Phase 3, which will give a much wider sense of the impact on, and possible side-effects for, people with dementia.”

There are 62,500 people with dementia in Scotland: that figure is set to rise to between 110,000 and 114,000 by 2031. Alzheimer Scotland’s 2007 report, The Dementia Epidemic - where Scotland is now and the challenge ahead, stated that:

The cost of dementia in Scotland in 2007 was between ￡1.5 and ￡1.7 billion. Dementia has a major impact on our economy.

These figures include the cost of accommodation (41% of total), informal care (ie the costs to family of caring) (36%), social work services (15%) and NHS care (8%). The estimated average cost per annum of a person with dementia is ￡25,472.

The cost of dementia in 2031 is projected to rise to ￡2.6 - ￡2.9 billion (at 2007 prices).

Alzheimer Scotland