Recent Alzheimer's Research

To follow up on comments on the culture of Alzheimer's research linked over at the Longevity Meme, I thought I'd point out some of the folk working hard to inject new ideas and theories into the field. You don't have to look far; quite a few interesting lines of research have reached the popular science websites in just the past few days:

Alzheimer's heart link explained:

Scientists have discovered how heart disease or a stroke may trigger Alzheimer's disease. Both conditions lead to a reduction of oxygen flow to the brain. A University of British Columbia team, studying mice, found this stimulates increased development of the protein clumps thought to cause Alzheimer's.


Scientists have known for some time that people with certain diseases that restrict their supply of oxygen, such as stroke or lung disorders, are more prone to Alzheimer's and also that people who live at high altitudes are also at greater risk of developing the disease. This research provides a molecular explanation for that anecdotal finding and shows that cues from cells, genes and a person's environment all play a role in causing this dreadful disease.

Nerve Fibers Need Specific Growth Factor Chemical To Form Connections Within The Brain:

The study uncovers how cholinergic neuronal circuits, which help the cerebral cortex process information more efficiently, rely on neurotrophin-3, a chemical that stimulates nerve growth. The scientists have determined the circuits need this chemical in order to recognize and reach their target nerve cells in the brain.


This finding, according to Robertson, has significant implications for neurodegenerative diseases like Alzheimer’s. Cholinergic neuronal circuits play a key role in the proper information processing by the cerebral cortex and other areas of the brain. The cerebral cortex is the part of the brain that determines intelligence, personality, and planning and organization, and these actions are compromised by neurodegenerative diseases.

“Studies on the brains of Alzheimer’s patients have shown a marked decline in these cholinergic circuits. Our work demonstrates that neurotrophin-3 is essential to maintain the connections to cerebral cortex neurons,” Robertson said. “This study shows that a neurotrophin-3 therapy may be able to induce nerve fibers to regrow in the cerebral cortex, which would be beneficial to people with Alzheimer’s.”

More insight into Alzheimer's disease with Stanford discovery of possible cause:

A peacekeeper in the body's defenses against infection may hold the key to understanding - and eventually treating - Alzheimer's disease. Researchers at the Stanford University School of Medicine discovered that when a molecule responsible for dialing down the immune system malfunctions in the brain cells of mice, the rodents develop symptoms of the degenerative brain disease.


Wyss-Coray and Ina Tesseur, PhD, an instructor in the Department of Neurology, examined thin slices of the brains of Alzheimer's patients who had died, and discovered abnormally low levels of a molecule involved in controlling the body's response to infection. That molecule allows the brain to detect and respond to TGF-beta, or transforming growth factor, a protein teeming through our bodies, involved in fighting infection, stopping cancer and perhaps keeping brain cells alive.

No other researchers had seen this change before, so Tesseur and Wyss-Coray set out to investigate whether it had some connection to Alzheimer's disease. They hypothesized that by protecting neurons, TGF-beta may help prevent Alzheimer's disease. If the TGF-beta pathway is turned off, the brain becomes more susceptible to a toxic buildup of proteins.

The problem with Alzheimer's - and most other complex biochemistry - is the matter of identifying what is the cause and what is the effect. It is to be expected that much of what has been discovered by researchers will fall to the wayside as a side-effect of the progression of Alzheimer's rather than an actual root cause. Equally, most of the therapies currently under development will turn out to be largely ineffective patching up of consequences rather than cures. Such is the way we forge into the unknown; understanding will come, as the scientific method is a powerful filter for effective solutions to any problem.

Is Alzheimer's actually a form of diabetes at root? Is it a failure of amyloid clearing mechanisms? Is amyloid even a cause, or is it a giant red herring and consequence of the real underlying biochemistry of the condition? It's a complex business - new ideas and broader exploration are certainly needed while the establishment forges ahead with consensus work on understanding and defeating the buildup of amyloid.

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I wish people were more careful using the term "Alzheimers", because that disease clearly has a genetic component and tends to strike people before they are 65 years of age. The kind of dementia being discussed in the article is clearly circulatory in nature, and should be called "circulatory dementia", not "Alzheimers". The reason for this is simple and should be obvious: persons with the Alzheimers gene(s) are much more likely to get the illness than any randomly selected person. There may be some interventions short of modifying their genotype that can reduce the probability, or delay the onset, but really in the end they need their genes "fixed".

Circulatory dementia, on the other hand, is likely a function of any of several circulatory problems, starting with high blood pressure & all the things that associate with it. As noted, it may be tied to diabetes (which affects blood pressure), it may be driven by plaque in arteries, etc. but we can intervene against it the same way we go after athlersclerosis.

Thus we have two categories of "Alzheimers", one genetic, one arguably preventable via some other means. That's not very good taxonomy! It leads to thinking in the wrong directions.

So let's call dementia induced by circulatory problems "circulatory dementia" or "dementia", not "Alzheimers". In this world of fuzzy terms, we need to use accurate and sharp words that convey an accurate meaning.

And thanks for the roundup on this topic.

Posted by: anonymous at November 21st, 2006 8:32 AM

I am 79 years old and have been diagnosed with MCI, mild cognitive impairment. I wonder whether any of the following may have been partially causative, such as:
- high altitude flying (up to 30,000 feet) as a USAF fighter pilot for two years,
- skiing at altitudes up to 10,000 feet, 50 to 100 days per year (in retirement),
- taking Cafergot for cluster headaches which narrows carotid arteries, up to 250 pills per year for 40+years.

Posted by: Dick Doner at September 10th, 2012 3:25 PM

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