Have we been wrong about what causes Alzheimer’s disease?
One of the major components of these protein buildups was thought to be a protein called amyloid beta, or Aβ42, which clump together into what is known as amyloid plaques.
“By the age of 85 years, only one fifth of those with amyloid plaques develop Alzheimer’s disease.”
“In the process of reacting, it transforms into amyloid plaques.
Once in amyloid, Aβ42 no longer works (the plaques can be viewed as a tombstone of Aβ42).”
Every single person living with Alzheimer’s disease has low levels of Aβ42 whereas many of us have amyloid plaques in our brain and are cognitively normal.”
“All stories have two sides—even the one we have told ourselves about how anti-amyloid treatments work: by lowering amyloid,” Espay said.
Traditional Banks: Learn the Differences So why do some people with high levels of amyloid plaques not see the cognitive decline associated with Alzheimer’s?
Do you have a question about Alzheimer’s disease?
Journal of Alzheimer’s disease : JAD, 90(1), 333–348.
According to new research, it appears that our understanding of the cause of Alzheimer’s disease may have been incorrect.
The buildup of aberrant proteins in and around our brain cells was the main theory for years explaining this neurodegeneration. Aβ42, also known as amyloid beta, was believed to be a major component of these protein buildups. This protein clumps together to form amyloid plaques. But this theory has been called into question by a recent University of Cincinnati study.
Alberto Espay, a neurology professor at the University of Cincinnati Academic Health Center, told Newsweek, “We noticed that most of the population with amyloid plaques does not develop Alzheimer’s.”. Only 25% of people with amyloid plaques by the age of 85 go on to develop Alzheimer’s disease. “. .
Further Reading: Newsweek Vault: What’s a Health Savings Account?
According to earlier studies conducted in Espay’s lab, these plaques are not the cause of Alzheimer’s directly. Rather, it seems to happen when Aβ42 levels are low.
“Our brain is protected by the protein Aβ42 against a range of harmful and infectious exposures,” explained Espay. Amyloid plaques are created during the reaction process. Amyloid plaques consist of Aβ42 clumps. Aβ42 stops functioning once it enters amyloid (the plaques can be thought of as Aβ42’s gravestone). “.
state that Alzheimer’s is a disease of loss: “We lose Aβ42,” stated Espay. Every single person with Alzheimer’s disease has low levels of Aβ42, but many of us are cognitively normal despite having amyloid plaques in our brains. “. .
The idea behind a lot of current Alzheimer’s treatments is that the disease is brought on by an accumulation of amyloid plaque. Espay added that the reduction in symptoms brought on by these medications might be a side effect.
Compare the Best Health Savings Account (HSA) Providers for More Information From Newsweek Vault.
Data from 26,000 participants in 24 randomized clinical trials examining the effects of novel Alzheimer’s treatments were examined by Espay and colleagues for a recent study that was published in the journal Brain. Cognitive impairment and variations in Aβ42 levels before and after treatment were evaluated in the trials. They discovered that following treatment, higher levels of Aβ42 were linked to a slower rate of cognitive decline.
“Every narrative has two sides, including the one we’ve told ourselves about the mechanism of action of anti-amyloid therapies, which is to reduce amyloid,” Espay stated. Indeed, they also cause an increase in Aβ42 levels. There might be a benefit even if this is an unintentional consequence. Our research demonstrates that variations in Aβ42 are at least as good as variations in amyloid in terms of predicting changes in cognitive outcomes in anti-amyloid trials. “.”.
Additional Newsweek Vault Content: Internet Banks versus. Know the Differences Between Conventional Banks.
How come some individuals with high amyloid plaque levels do not experience the cognitive decline linked to Alzheimer’s disease? “We found that the ability to produce enough Aβ42, a critical protein for brain health, to maintain it within normal levels keeps people with amyloid plaques cognitively normal,” explained Espay.
Future treatments for Alzheimer’s disease may benefit from these discoveries. “If the problem with Alzheimer’s is the loss of the normal protein, then increasing it should be beneficial, and this study showed that it is,” Espay said. “The narrative makes sense: it is preferable to raise Aβ42 levels to within the normal range. “.”.
Please send us an email at health@newsweek . com if you have any questions or concerns about Alzheimer’s disease. We can consult specialists, and Newsweek might publish your story.
Citations.
The Sturchio, A. Dwivedi, AA. K. Malm, T. Wood, Miss J. A. . J., Sharma, R., and Cilia. Hill, E.; Sdot. H. Schneider, Leonard. Graff-Radford, N.; Sdot. H., R., and Mori. Nübling, G. El Andaloussi, S.; P. Svenningsson. Ezzat K. Espay, A. J. together with the Dominantly Inherited Alzheimer Consortia (DIAN) (2022). Amyloid-positive individuals with mutations causing Alzheimer’s disease are predicted to have normal cognition based on high soluble Amyloid-β42. 333–348 in Journal of Alzheimer’s Disease: JAD, 90(1). https://doi.org/10.3233/JAD-220808.
