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News for the Week of Apr 25, 2006

Phase I Trials for NP031112

(Source: Europa Press) - Neuropharma announced Phase I clinical trials for NP031112, the company's first medicine to treat Alzheimer's disease.

The NP031112 molecule acts as an inhibitor of GSK3 (also known as tau protein kinase I) and has received the approval of the German authorities to begin Phase I clinical trials to develop an agent to treat Alzheimer's disease.

The trials will consist of two stages, testing the drug (1) in phased single doses, and (2) in repeated doses for seven days.

For more information contact Manuel de la Cruz

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PSA Lets You Listen to Alzheimer's Patients

(Source: TransWorld News) - In Los Angeles, radio listeners can eavesdrop on a chilling conversation between an Alzheimer's patient and her son as part of a new Alzheimer's Association public service announcement (PSA).

The 30-second PSA begins with ominous music and a frightened older woman saying, "Who are you? Who are you?!" Her son's reply, "Hi mom, it's me."

In just ten syllables, the terror of Alzheimer's is conveyed.

The commercial ends with an invitation to help in the fight against Alzheimer's disease and directs people to visit the Alzheimer's Association Web site (

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Where to Turn When Seniors Need Help

(Source: - When an older family member needs help related to health and a living situation, where can they turn and where do they start?

One answer is to contact service providers; information, referral and assistance programs; or to try web sites or Internet-based employee assistance programs that many jobs provide.

Sandra J. Cohen, R.N., and Roger Cormier, elder care managers, suggest a few tips for finding what you need:

  • Find a resource that will provide more than just a list. You need to learn why that list is appropriate for you and how to narrow down and evaluate the providers on the list.
  • Do your homework and trust your gut feelings. Get at least a second opinion from somebody who knows the situation. If you can, try a program or service before making a long-term commitment. For example, don't sell your house if you don't have to until you settle in and decide that your new assisted living arrangement will work for you.
  • Be realistic about your options. Just as with other aspects of your life, you seek what is right for you, not what is guaranteed to be perfect.
  • If you get discouraged, ask someone to help you get started on your search again. It's not necessarily your problem that you had trouble navigating around a vast, unfamiliar network of services.

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To Tell or Not To Tell Mother - Dad Died

(Source: - A Dear Abby readers writes, "Mom, who is in the middle stages of Alzheimer's, once told me that she thought my father (who had died 10 years before) was having an affair because his shoes were not in the closet. Also, some other woman's clothes' were in there. (We had added a few new items to Mom's wardrobe.)"

"I very hesitantly began to remind my mother how sick Dad had been, and finally worked around to saying that he had died 10 years ago. My mother's response: 'Well, THAT'S a relief!'"

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Friends & Family Reduce Damage from Alzheimer's

(Source: Rush University Medical Center) - According to a Rush University Medical Center study, having close friends and staying in contact with family members offers a protective effect against the damaging effects of Alzheimer's disease.

The study found that the amount of Alzheimer's disease pathology and cognitive performance changed with the size of a person's social network. Basically, the more support from family and friends, the less cognitive impact of the disease.

While other studies have shown people with more extensive social networks were at reduced risk of cognitive impairment, this study is the first to examine the relations between social networks and Alzheimer's disease pathology.

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Is Mild Cognitive Impairment a Part of Normal Aging?

(Source: Doctor's Guide) - In a round-table presentation at the 9th International Symposium on Advances in Alzheimer Therapy, Dr. Jodey Corey-Bloom began by saying that much depends on the definition of mild cognitive impairment (MCI) - whether it is considered a normal part of aging or a clinical entity worthy of treatment.

"The concept of MCI at its core is really cognitive impairment without dementia", she said.

Professor Corey-Bloom added that the most compelling evidence is that the neuropathology of aMCI (MCI accompanied by the genetic APOE4 allele) does indeed parallel very early AD.

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Study Provides a New Look at Alzheimer's Disease

(Source: Buck Institute) - There are approximately 200 mice at the Buck Institute in Novato, CA, that have all the pathological signs of Alzheimer's, but no memory loss or other symptoms of the disease. Despite the fact that their brains are loaded with sticky deposits commonly associated with the neurodegenerative disease, they have normal memories, and show no brain shrinkage or neuronal damage.

The Buck scientists, led by Veronica Galvan, believe that what saved the mice from their neurodegenrative fate was blocking a molecular pathway that is a critical for the development of the disease - the last 31 amino acids in the APP (amyloid precursor protein) sequence, called C31.

"This research casts a totally new light on Alzheimer's disease," said Dale Bredesen. "The current thought is that Alzheimer's is a toxic disease, with the amyloid plaques acting as a 'bomb' that destroys neurons. In actuality, AD may be a more subtle disease, which develops when the normal process of nerve signaling goes out of balance."

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A Manual to Help Dementia Caregivers in Scotland

(Source: The Press and Journal) - Alzheimer Scotland ( and NHS Health Scotland is offering "Coping with Dementia: A Practical Handbook for Carers," to help those who look after people with moderate to late-stage dementia.

Kate Fearnley, co-author of the booklet, said that the booklet "looks at all the different effects dementia may have and explains to carers how to deal with them."

For more information go to

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Does Telomere Shortening Predict Dementia?

(Source: DocGuide) - Despite previous reports, study findings reported at the International Symposium on Advances in Alzheimer Therapy (Geneva, Switzerland), indicate that telomere length cannot be used to predict dementia.

Principal investigator Dr. Dina Zekry explained that telomeres are short, repeated DNA sequences, some of which become lost in normal cell duplication.

"The telomere hypothesis of aging is based on the notion that telomere shortening with each cell division, and therefore with age, results in cell senescence," Zekry said.

As senescent cells contribute to aging, telomere length might be considered as a potential biomarker of aging, she added. This thus led to the "telomere hypothesis of dementia," that asks whether telomere shortening contributes to the genesis of certain age-related diseases, such as dementia. For more information on the telemere hypothesis of aging click here.

Zekry and colleagues conducted a 1-year longitudinal study to investigate telomere length and if it could predict dementia in very elderly patients. They found that telomere lengths in both the dementia and non-dementia patients showed no significant decline with age.

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Phospholipase D1, BetaAPP Trafficking in Familial AD

(Source: PharmaReport) - Mutations in the PS1 gene have been linked to the genetic form of Alzheimer's disease. In this study, conducted at Rockefeller University in New York, scientists found that a PS1-interacting protein, phospholipase D1 (PLD1), affects intracellular trafficking of beta-amyloid precursor proteins (betaAPPs) The results indicate that PLD1 may represent a therapeutic target for rescuing compromised neuronal function in AD.

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Physiological, Biochemical & Molecular Alterations in AD

(Source: DocGuide) - In a round-table discussion at the International Symposium on Advances in Alzheimer Therapy, Dr. Paul Francis asked, "Does the current approach to treatment of Alzheimer's disease fit our current understanding of the physiological, biochemical and molecular alterations that occur as a result of this disease?"

The round-table meeting, entitled "Controversies in cholinergic therapy for mild cognitive impairment and Alzheimer's disease," compared disease-modifying agents to symptomatic agents and how these different modifying strategies are promoting a broadening approach to the treatment of Alzheimer's disease.

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Posiphen Helps Stem Cells Fight AD

(Source: UPI) - Researchers at the University of Central Florida report that the drug Posiphen could enhance the results of using stem-cell transplants to treat Alzheimer's disease.

The scientists found that when they pre-treated transgenic Alzheimer's mice with Posiphen, the human neuronal stem cells (HNSCs) began to differentiate into neurons in the brain. In contrast, the stem cells transplanted into the brains of mice not treated with the drug failed to differentiate into neurons.

The researchers surmised that these outcomes were due to the fact that Posiphen seems to suppress a key protein known as the amyloid precursor protein (APP), allowing production of new neurons in the brain.

Posiphen is undergoing a Phase I clinical trial by the drug maker Axonyx for the potential treatment of Alzheimer's progression.

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CoQ10 May Protect Against Alzheimer's

(Source: NutraUSA) - Researchers from Hamdard University, John Hopkins University and the University of South Carolina report preliminary findings suggesting that increased intake of the anti-oxidant co-enzyme Q10 (CoQ10) may help ward off the threat of Alzheimer's disease.

Although the mechanism of Alzheimer's disease remain unclear, one widely accepted theory is that it is due to a build-up of amyloid plaque deposits. These deposits have been associated with an increase in brain cell damage and death from oxidative stress.

CoQ1 has been shown to help prevent Parkinson's disease.

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A Report on the Alzhemed Clinical Trial

(Source: - At the International Symposium on Advances in Alzheimer Therapy, Dr. Paul S. Aisen reported findings from an Alzhemed study announcing that stabilization of the disease occurred in four out of nine patients with a mild form of AD after three years of treatment.

"Overall, the Alzhemed program is very exciting. The fact that this product can reduce amyloid accumulation, a major culprit in Alzheimer's disease, and provides a protective effect against amyloid-induced toxicity to brain cells is encouraging," said Aisen.

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