Souvenaid and Alzheimer’s Disease

Souvenaid, in its second clinical trial, has been proven to help the memory of people who suffer from mild Alzheimer’s disease (AD). Results of the trial were given at the 4th International Conference on Clinical Trials in Alzheimer’s Disease (CTAD) by Philip Scheltens, MD, PhD in San Diego in early November. Scheltens is head of the Alzheimer Center at the VU University Medical Center in Amsterdam.

Souvenaid has a unique mixture of nutrients that work by stimulating the connections between nerves, also known as synapses. Losing these connections is what many experts think is responsible for losing memory in Alzheimer’s patients.  Studies demonstrate that the nutrients in Souvenaid can help grow new synapses in the brain. People taking Souvenaid daily over three months had improved scores on memory tests.

Scheltens is cautiously optimistic about the new findings. More research needs to be done before any conclusions can be drawn, but he thinks it is a step in the right direction.

Souvenir II was completed at  27 centers in six countries in Europe to see if the effects from Souvenir I would last for eight weeks. This study used additional measures to test for recall and also measured brain activity. Of 259 subjects, over 91% finished the study.

Memory was tested at the beginning, at 12 weeks, and at 24 weeks. The composite score was gotten from the Rey Audtiory Verbal Test which tests instant recall, delayed memory, and recognition. The Wechlser Scale which tested verbal association was also used.

Over the 24 weeks, the total scores from the Souvenaid group were much higher than those from the control group. Besides just looking at memory scores, they are attempting to analyze the electroencephalogram and magnetoencephalogram data, which may help figure out the influence  Souveniad has on synapse building in patients with Alzehimer’s disease and dementia.

CTAD is sponsored by the University of California, San Diego School of Medicine and the European Alzheimer’s Disease Consortium (EADC).

Possible New Drug for Alzheimer’s Disease

Taken orally, E64d, a type of cysteine pro-tease inhibitor, has shown to reduce the buildup of β-amyloid (Aβ) present in animal model brains used in Alzheimer’s disease studies. This action resulted in significant improvement in memory loss. The findings were discovered by a group of researchers from the American Life Science Pharmaceuticals-San Diego, University of California-San Diego and the Medical University of South Carolina. Their findings will be published in the Journal of Alzheimer’s Disease in the September issue.

Dr. Vivian Y.H. Hook praises the discovery since according to her, E64d has been proven safe for human consumption and that the results of the research has excellent potential for use in the treatment of Alzheimer’s disease.

It is known that there is a co-relation in the increase in the levels of Aβ peptides, amyloid plaques and the onset of loss of memory. Aβ peptides are separated from the APP or amyloid precursor protein by the β-secretase. The peptides later develop plaques in the regions of the brain associated with memory.

E64d reduces the level of Aβ by blocking the β-secretase from taking apart the amyloid precursor chain. However, researchers also discovered that it also increases BACE1 activity, a protease known as the principal β-secretase. E64d seems to decrease Aβ in the lower brain by blocking the β-secretase activities of Cathepsin B, another protease.

According to Hook, the study shows that Cathepsin B may be used for the inhibition of the production of Aβ and the resulting improvement of memory function. The finding is important since inhibition of β-secretase and Cathepsin-B is possible without the inhibition of BACE1.

The research involved the use of young and old mice with transgenic Alzheimer’s. Young mice fed with E64d avoided memory loss while old mice showed improved memory.

The study is not new — it actually used a previous work where Cathepsin B was also utilized for memory enhancement. In that study published in 2008, though, Cathepsin B inhibitors were directly administered into brains of mice with AD. The recent study shows that oral administration was effective and could pave the way for future human clinical trials.

The study is co-authored by Dr. Gregory Hook of San Diego’s American Life Science Pharmaceuticals and Dr. Mark Kindy of the Medical University of South Carolina, the Ralph H. Johnson VA Medical Center, and Applied Neurotechnology, Inc. in Charleston, SD. The recent study also received some support from the National Institutes of Health and the Alzheimer’s Drug Development Foundation’s National Institute on Aging.

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In this, the third of our series of breakthrough tests for Alzheimer’s disease, scientists at the University of California San Diego (UCSD), have developed a fast and accurate method for quantifying subtle, sub-regional brain volume loss using magnetic resonance imaging (MRI). This study promises to improve diagnosis and monitoring of Alzheimer’s disease (AD).

The techniques were applied to the dataset of the multi-institution Alzhiemer’s Disease Neuroimaging Initiative (ADNI). What the scientists at UCSD were able to demonstrate was that the sub-regional brain volume measurements outperform available measures for tracking the severity of AD, including widely used cognitive testing and measures of global brain-volume loss.

According to insciences.org, the new research shows that changes in the brain’s memory regions, in particular a region of the entorhinal cortex, offer sensitive measures of the early stages of the disease. According to Anders M. Dale, PhD, professor of neurosciences and radiology at the UC San Diego School of Medicine, who led the study, “Loss of volume in the hippocampus is a consistent finding when using MRI, and is a reliable predictor of cognitive decline. However, we have now developed and validated imaging biomarkers to not only track brain atrophy, but distinguish the early stages of Alzheimer’s disease from changes related to normal aging.”

The study’s co-author, James Brewer, MD, PhD, a neurologist and assistant professor in the Departments of Radiology and Neurosciences at UCSD adds that, “The technique is extremely powerful, because it allows a researcher to examine exactly how much brain-volume loss has occurred in each region of the brain, including cortical regions, where we know the bad proteins of Alzheimer’s disease build up.”

If a picture is worth a thousand words, here are serial MRI brain scans, taken six months apart, that show progression from mild cognitive impairment to Alzheimer’s disease with significant atrophy (blue) and ventricle enlargement (orange/red).

For more information, see “Analyzing Structural Brain Changes in Alzheimer’s Disease” at insciences.org.

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Mount Sinai Sch of MedFrom the Mount Sinai School of Medicine on the Upper East Side of New York City comes exciting news that it is one of 12 sites nationwide participating in the first Phase 2 clinical trial to test gene therapy treatment for Alzheimer’s disease (AD). The study is the first multicenter neurosurgical intervention in Alzheimer’s research in the U.S. The Alzheimer’s Disease Cooperative Study (ADCS) is sponsoring the study through a grant from the National Institute on Aging (a part of the National Institutes of Health [NIH]) in association with Ceregene, Inc., which developed and will provide the active agent (CERE-110).

According to Mount Sinai’s press release:

The experimental treatment utilizes a viral-based gene transfer system, CERE-110, that makes Nerve Growth Factor (NGF), a naturally occurring protein that helps maintain nerve cell survival in the brain. CERE-110 has been previously studied in animals, where it reversed brain degeneration in aged monkeys and rats. For this study, CERE-110, will be injected by a neurosurgeon directly into the nucleus basalis of Meynert (NBM) of the brain, an area where neuronal death occurs in Alzheimer’s patients.

Mount Sinai Medical Center

Mount Sinai Medical Center

In animal studies, NGF has been shown to support the survival and function of the neurons that deteriorate in Alzheimer’s patients. These neurons produce the chemical acetylcholine, which is important in memory and cognitive function. The hope is that improvement of this system’s function may lead to better memory performance in Alzheimer’s patients.

Participants in the Phase 2 study will be randomly placed into one of two treatment groups, with half receiving CERE-110 via neurosurgery and half receiving placebo surgery without any cranial injections. Once the study is completed, and if the results are promising, participants in the placebo group will be eligible to be treated with CERE-110. All participants will receive a thorough medical examination and cognitive testing. In addition, participants will be closely monitored by a team of physicians for the duration of the two-year study. Participants will also be encouraged to participate in long-term follow-up.

The Phase 1 study in Alzheimer’s patients was conducted at Rush University in Chicago and the University of California San Diego. Researchers observed increases in brain metabolism in several cortical regions of the brain at 6- and 12-month follow-up in some of the participants. With follow-up ranging from six months to more than four years post-treatment, there have been no side effects thought to be caused by CERE-110.

For more information from ADCS, click here. More information is also available at National Institute on Aging’s Alzheimer’s Disease Education and Referral Center (ADEAR). Click here.