In 1906, a gathering of psychiatrists in Tbingen, Germany was told about a strange disease process of the cerebral cortex.
A 50-year-old woman with memory loss, delusions, hallucinations, aggression, and confusion died five years after she was diagnosed with the disease.
Alzheimer's brain was found to have plaques on it. The plaques are believed to be the cause of Alzheimer's disease.
The theory has a couple of problems.
It doesn't explain why people with plaques in their brains don't have any neurological symptoms.
There have been unsuccessful trials for drugs that reduce plaques.
The original form of the amyloid-betaProtein is lost when it accumulates in the form of plaques.
Patients have worse clinical outcomes when their levels of amyloid-beta are reduced.
The amount of plaques in the brain is more important for Alzheimer's disease progression than the amount of amyloid-beta 42 remaining.
We studied data on a group of people with rare inherited genes that put them at high risk of Alzheimer's disease. The participants were part of the study.
The amount of plaques is less harmful than the amount of amyloid-beta 42.
We found that participants with high levels of amyloid-beta 42 in their cerebrospinal fluid were protected and their cognitive abilities were preserved over the three year follow up.
Many studies show the functions of amyloid-beta 42 in memory and cognitive functions.
The strongest evidence supporting the idea that amyloid-beta plaques are harmful is found in a group of people who have a genetic variation that makes them more prone to Alzheimer's.
Even though there were plaques in the brains of those with higherCSF levels, they were still able to function normally.
In some rare forms of Alzheimer's disease, people can develop dementia if they have low levels of amyloid-Beta 42 and no plaques.
This suggests that plaques are not the cause of dementia.
What will our findings do for Alzheimer's disease research? All the drug trials for Alzheimer's disease have failed because of lecanemab.
Drugs were designed to reduce the levels of amyloid-beta 42 in order to reduce the number of plaques. The drugs made the patient worse.
Lecanemab has been reported to reduce cognitive decline. The drug increases the levels of amyloid-beta 42 in the brain.
This is in line with our hypothesis that the increase of the normal amyloidProtein can be beneficial.
The results of the trial will be published. The only thing we have is a press release from the drug's makers.
It will be important for future trials to focus on the levels of amyloid-beta 42, and whether it is beneficial to increase and restore its levels to normal values, rather than targeting it for removal.
The natural amyloid-beta 42 clumps together more than the "protein analogs" used for this.
This approach could become a promising new avenue of treatment for Alzheimer's and other related diseases.
Research Scientist, Laboratory Medicine, and Professor, Laboratory Medicine, are two of the people mentioned.
Under a Creative Commons license, this article is re-posted. The original article is worth a read.
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