What causes Alzheimer’s disease? New research looks promising for patients

A psychiatrist and neuroanatomist in 1906. Alois Alzheimerto a meeting of psychiatrists in Tübingen, Germany, “ a specific severe disease process of the cerebral cortex He reported an incident that he introduced as ”. The Incident was betting on a 50-year-old lady suffering from memory loss, delusions, hallucinations, aggression, and confusion, and all the symptoms deteriorated until she passed away five years later.

At autopsy, Alzheimer’s noticed obvious plaques in his brain. These plaques, identified as aggregates of amyloid-beta proteinIt is still considered the cause of Alzheimer’s disease.

However, there are two important problems with this theory. The first of these problems does not explain why many subjects (even the elderly) have plaques in their brains in the absence of any random neurological symptoms such as memory loss. Second, clinical trials for drugs that reduce these plaques have failed (with one last exception).

When amyloid-beta proteins build up as plaques (insoluble clumps), the brand new soluble form of the protein that performs valuable functions in the brain is consumed and lost. Some studies show that low levels of soluble amyloid-beta, called amyloid-beta 42, lead to worse clinical outcomes in patients.

What causes Alzheimer’s?

Researchers from the Karolinska Institutet Clinical Neuroscience PhD Student Medical Physician Andrea Sturchio, Laboratory Medicine Research Scientist Kariem Ezzatand Professor of Laboratory Medicine Samir EL Andaloussi’In a recent study published in the Journal of Alzheimer’s Disease, it was investigated whether the measure of plaque in the brain or the remaining measure of amyloid-beta 42 was more valuable to the progression of Alzheimer’s disease.

To answer this question, we analyzed data on a cluster of human beings with a rare inherited gene mutation at high risk of developing Alzheimer’s disease. associates, Retrieved from the Dominantly Inherited Alzheimer’s Network cohort study.

In this study, depletion of Amyloid-beta 42 (the functional version of amyloid-beta) was found to be more disproportionate than the extent of plaques (insoluble clumps of amyloid beta).

Participants were followed for an average of three years, and those with high levels of amyloid-beta 42 in their cerebrospinal fluid (fluid around the brain and spinal cord) were found to be preserved and their cognition preserved throughout the study period. These results were in agreement with many studies showing the valuable functions of amyloid-beta 42 in memory and cognition.

It’s also said that people with low, inherited forms of Alzheimer’s disease can develop dementia with low amyloid-beta 42 levels and no detectable plaques, according to the study, suggesting that plaques are not the cause of dementia, but low amyloid-beta 42 levels.

New hope for Alzheimer’s patients

These findings could have a valuable impact on drug development and clinical trials for Alzheimer’s disease. As mentioned, L, an antibody drug that reduces plaques ecanemabAll drug trials in Alzheimer’s disease have failed, until the last trial with

Some drugs were designed to reduce amyloid-beta 42 levels based on the rationale that patients would accumulate less plaque if their usual protein levels were reduced, but these drugs often made the patient’s condition worse.

Lecanemab was recently reported to have a small but valuable effect in reducing cognitive decline. Compared to previous studies, this drug Increases amyloid-beta 42 levels in CSFand this, once again, is in line with the hypothesis proposed in the study that an increase in usual amyloid protein may be beneficial.

In other words, focusing future trials on amyloid-beta 42 levels and examining the effect of increasing these levels may offer a new avenue of treatment for Alzheimer’s disease and other protein aggregation diseases.

Detailed results of the lecanemab trial will be announced in more detail in the near future.