Researchers in Iceland identified a rare genetic mutation that slows the activity of an enzyme called beta secretase, which is required to produce amyloid-beta.
As a result, the concentration of amyloid-beta increases and begins to form deposits, known as amyloid plaque, in the brain.
The next year Golde, at the Mayo Clinic, and his collaborator Edward Koo, at uc, San Diego, showed--at least in the test tube--that high doses of ibuprofen and other anti-inflammatories could lower production of amyloid-beta-42, which was believed to be a bad type of amyloid.
The idea that more brain cell activity could lead to more amyloid-beta build up is an exciting, if sobering, finding.
FORBES: Wandering into Alzheimer's: Could Your Thoughts Reduce Your Risk?
These findings strongly link increasing neural activity to the buildup of amyloid-beta.
FORBES: Wandering into Alzheimer's: Could Your Thoughts Reduce Your Risk?
Most researchers are focusing on blocking the formation of amyloid-beta protein or removing it from the brain, either before or after deposits are formed.
Oligomers, which are considered more toxic to brain tissue than amyloid-beta proteins, were applied to the hippocampus, the brain's memory center, in young mice.
In the current study, his team found that there was more amyloid-beta accumulation during the night hours, when mice are typically awake, compared to daytime hours.
FORBES: Wandering into Alzheimer's: Could Your Thoughts Reduce Your Risk?
Harvard University researchers conducted experiments on mice using oligomers, a soluble form of amyloid-beta protein, which is the key compound in brain plaque and a hallmark of Alzheimer's.
Amyloid-beta is a precursor of full-blown plaques and, ultimately, dementia.
FORBES: Wandering into Alzheimer's: Could Your Thoughts Reduce Your Risk?
Using mice as subjects, the team found that the more lactate was present in certain areas (lactate is a product of neuronal activity), the more amyloid-beta peptide was also present.
FORBES: Wandering into Alzheimer's: Could Your Thoughts Reduce Your Risk?
While the primary endpoints of the two pivotal studies conducted were not met, a secondary analysis of the data demonstrated that a molecule acting specifically on amyloid-beta can slow cognitive decline in patients with mild AD.
And while researchers continue to explore how we can reduce amyloid-beta levels in the brain (whether by changing behaviors, thought processes, or by pharmacological methods), the best advice is probably to stay as cognitively active as you can, get some rest, and perhaps most importantly, be as happy as you can be.
FORBES: Wandering into Alzheimer's: Could Your Thoughts Reduce Your Risk?
If beta amyloid is the key to stopping Alzheimer's, dimebon shouldn't work at all.
Beta amyloid is a protein fragment that collects in clumps inside the brains of Alzheimer's patients.
One large area of research is in plaques of beta amyloid which form on the brain.
Elan's other approach would be to inject patients with antibodies for beta amyloid made outside the body.
But we don't know if what is lighting up is tau alone, or beta amyloid, or both.
Levels of the beta amyloid protein naturally rise and fall over 24 hours in both mice and people.
Gandy decided to look at another reputed culprit in Alzheimer's called beta amyloid.
As expected, the vaccine created antibodies that prevented beta amyloid plaques from forming.
Perhaps these compounds will finally prove or disprove the beta amyloid hypothesis.
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It binds not just to tau, but also to another protein called beta amyloid, which is commonly seen in Alzheimer's disease patients.
Beta amyloid forms sticky plaques in the brains of Alzheimer's patients and many scientists suspect that slowing plaque formation could slow the disease.
AN-1792 was a vaccine that immunized patients against a protein called beta amyloid, which is the main component of the plaques that destroy the brain in Alzheimer's disease.
The antibodies seem to respond to only a quarter of the beta amyloid molecule, and the rest of the molecule seems to call the T cells into action.
Given that bapi seems to be effective in lowering AD biomarkers such as beta amyloid and phospho-tau, perhaps bapi needs to be administered to patients at an earlier stage.
FORBES: For Pfizer-JNJ Alzheimer's Drug, It May Be Too Late To Try
The main anatomical symptoms of Alzheimer's are the growth in the brain of plaques of a protein called beta amyloid, and tangles inside cells of a second protein called tau.
The dominant explanation of Alzheimer's disease contends that the massive brain cell death is due to the buildup of plaques containing a protein called beta amyloid built up in the brain.
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