More On Alzheimer's Research

On current Alzheimer's study involves trying out gene therapy to boost neural growth:

In Alzheimer's disease, there is a die-off of brain cells involved in memory and cognition. The goal of gene therapy is to boost production of a naturally occurring protein, called nerve growth factor, that prevents cell death and helps neurons grow new connections, said Dr. Zoe Arvanitakis, co-director of the study.

The gene is delivered by a fragment of a harmless virus. The surgeon delivers a few drops, containing about 1 billion viral fragments, deep into the brain. It's hoped the viral fragments will invade brain cells and deliver the gene. The gene then would direct the cells to produce the nerve growth factor.

Gene therapy has been tried for other diseases, including cystic fibrosis, cancer and Parkinson's disease. But many efforts have failed, and no gene therapy has been approved for general use outside of clinical trials.

The Rush trial is the second study of the Alzheimer's gene treatment, called CERE-110. An earlier study of eight patients at the University of California-San Diego found that CERE-110 is generally safe. The Rush study is using a different mechanism to deliver the gene.

If this works, it could prove useful in combination with some way to prevent the ongoing damage mechanisms of Alzheimer's. Randall Parker has the details on just such an attempt (that I also noted recently at the Longevity Meme):

Antibodies injected into a small number of Alzheimer's Disease (AD) patients appear to have stopped the progression of Alzheimer's by attacking the plaques assocated with the disease.

Immunoglobulins which are already being used to treat multiple sclerosis may also be able to help patients with Alzheimer's. This, at least, is the finding of a pilot study on five patients at the University of Bonn. The results are set out in the forthcoming edition of the Journal of Neurology, Neurosurgery and Psychiatry (vol. 75, pp. 1472-1474), which also devotes its editorial to this discovery.

Immunoglobulins contain, among other things, anti-bodies against a protein which is the 'main suspect' thought to trigger off Alzheimer's. After six months of immuno-globulin doses the concentration of this protein in the patients' cerebrospinal fluid was reduced by one third. The patients' cognitive abilities improved slightly.

Studies also show that exercise - mental and physical - reduces the risk of suffering Alzheimer's as well as other common age-related degenerative conditions.

The health benefits of regular walking may include helping prevent mental decline and Alzheimer's disease, research in patients aged 70 and up has found, bolstering evidence that exercise needn't be strenuous to be good for you.

There's plenty of evidence that mental exercise, such as crossword puzzles and reading, may reduce Alzheimer's risks, but previous studies on brain benefits from physical exercise had conflicting results.

The new findings, contained in two studies, clarify how much exercise might be beneficial and are good news for older people who want to avoid mental decline but "don't like doing all that awful, sweaty stuff," said Bill Thies, vice president for medical and scientific affairs of the Alzheimer's Association.

Any effective therapy for Alzheimer's will save a great deal of money - both for individuals and socialized medical systems. While saving money is not high on the list of ethical reasons to save lives, it is what motivates organizations to action:

A new report has found that delaying the onset of new dementia cases by as little as five months could save the [Australian] community more than $1 billion.

As I've said before, preventing or developing cures for neurodegenerative conditions is vital to the process of greatly extending the healthy human life span.

Comments

I find the prospect of both gene therapy and the use of Ig in the future treatment of the widely alzheimers afflicted public hopeful (if not promising. The question(s) I would like to pose, however, is/are how might Ig be used in a way as to not promote encephalitis and possibly in synergy with gene therapy, antioxidant treatment and/or turning off of the recptor in the newly determined ligand binding mechanism of Amyloid Beta molecules? I am curious as to the latest research findings (collectively) that you can share, as well as your own thoughts (from the experts in their relative fields)on the possible implications of current findings as well as possible future treatment modalities. I am just a humble biology student in a community college and would like to know more about a disease that I have researched extensively (relevant literature and exhaustive questions to my professors and to legitimate online resources). I am aware of PET findings, SPECT findings, and am well acquainted with gene therapy; additionally the role of free radicals in apoptopsis (in a necessary way) as well as the detriment these oxygen species cause to cells. What I am seeking (almost despeartely you may say) is new information and more importantly strong hypothesis and theories relating to current research. Thank you for your patience and help in this matter from the extensive catalogue of your knowledge and expertise

Posted by: Jacob Mack at February 2nd, 2005 10:38 AM

I find the prospect of both gene therapy and the use of Ig in the future treatment of the widely alzheimers afflicted public hopeful (if not promising. The question(s) I would like to pose, however, is/are how might Ig be used in a way as to not promote encephalitis and possibly in synergy with gene therapy, antioxidant treatment and/or turning off of the recptor in the newly determined ligand binding mechanism of Amyloid Beta molecules? I am curious as to the latest research findings (collectively) that you can share, as well as your own thoughts (from the experts in their relative fields)on the possible implications of current findings as well as possible future treatment modalities. I am just a humble biology student in a community college and would like to know more about a disease that I have researched extensively (relevant literature and exhaustive questions to my professors and to legitimate online resources). I am aware of PET findings, SPECT findings, and am well acquainted with gene therapy; additionally the role of free radicals in apoptopsis (in a necessary way) as well as the detriment these oxygen species cause to cells. What I am seeking (almost despeartely you may say) is new information and more importantly strong hypothesis and theories relating to current research. Thank you for your patience and help in this matter from the extensive catalogue of your knowledge and expertise; sincerely,Jacob Mack.

Posted by: Jacob Mack at February 2nd, 2005 10:39 AM

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