As a result, the concentration of amyloid-beta increases and begins to form deposits, known as amyloid plaque, in the brain.
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.
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.
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.
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.
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?
Prions, beta-amyloid and synuclein, by contrast, are full of sticky structures called beta-sheets that react willy-nilly with crucial proteins.
The treatment also eliminated damage linked to the build-up of beta-amyloid.
Researchers are still trying to prove the beta-amyloid theory as the cause of AD.
The kinds of tests that would detect beta-amyloid levels are not widely available.
Most scientists believe that Alzheimer's disease is linked to a protein called beta-amyloid.
It trained the patient's own immune system to attack a protein called beta-amyloid that many scientists believe is implicated in Alzheimer's.
Other researchers had identified several related protein fragments, called beta-amyloid, inside the amyloid plaques, but they didn't know which proteins were the bad ones.
The team also looked at levels of beta-amyloid in the brains.
They used a modified version of the HIV virus to transfer a gene for neprilysin to neurons of genetically modified mice which produced human beta-amyloid.
In 1993 Lansbury showed that when he put a smidgen of beta-amyloid-42 into a mixed solution of free-floating amyloid particles, it immediately caused them to coalesce into clumps.
Most researchers still believe beta-amyloid is the culprit, but the idea that free-floating protein molecules, rather than the proteins in the plaques, are to blame is gaining ground.
The physical manifestations of the disease that Alois Alzheimer noticed in 1906 are sticky plaques of one type of protein, now known as beta-amyloid, and nerve-cell-engulfing tangles of a second type, called tau protein.
Despite the fact that other inhibitors of beta-amyloid have failed in clinical trials, Roche is moving ahead with gantenerumab to see if early intervention in patients at risk for AD can stave off disease.
This idea is supported by a study published in April in the Annals of Neurology, which showed that mice without plaques, but with floating beta-amyloid, were just as weakened by the disease as mice with both.
To be specific, Merck (MRK) will test a beta-amyloid precursor protein site-cleaving enzyme, or BACE, inhibitor, which the drugmaker notes is the first drug with this type of mechanism to advance to this stage of clinical research.
"There is a 50-60 percent decrease in the amount of amyloid plaques and indeed the amount of a-beta proteins in the brains of mice who have gotten chronic nasal treatment, " their report said.
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