How is Alzheimer’s progressing?
The role of so-called neuroinflammation in the development of Alzheimer’s has been investigated in a recent study – with quite surprising results. Neuroinflammation appears to be the main cause of the proliferation of pathologically misfolded proteins in the brain and to cause cognitive impairment in people with Alzheimer’s disease.
A study on living people has now found for the first time that neuroinflammation – the activation of immune cells located in the brain, known as microglial cells – is not simply a result of the progression of Alzheimer’s. Rather, it is an important upstream mechanism that forms the basis for the development of the disease, University of Pittsburgh researchers report the results of their current study. The study was published in the English-language journal “nature medicine“Published.
What happens in the brain in Alzheimer’s disease?
Alzheimer’s Characterized by the accumulation of so-called amyloid plaques in the brain. These are protein aggregates that are deposited between the nerve cells of the brain. Another feature of Alzheimer’s disease is the accumulation of so-called tau tangles, or tau proteins, that build up inside nerve cells, according to the team.
Although studies on cultured cells and laboratory animals have already provided much evidence that activation of microglia drives the proliferation of tau fibers in Alzheimer’s disease, this process has not yet been proven in humans, according to the researchers.
Curb neuroinflammation to prevent dementia
Study results suggest that targeted control of neuroinflammation is beneficial for people with early Alzheimer’s disease and may help prevent or reduce the accumulation of pathological tau proteins in the brain and prevent dementia, experts report in a recent study. Press release Der University of Pittsburgh School of Medicine.
Neuroinflammation more common in people with Alzheimer’s disease
To determine the exact mechanism by which distorted knots of tau protein fibers and amyloid plaques spread in the brain and lead to dementia, experts used live imaging to examine the brains of people who already had dementia. There are different stages of Alzheimer’s disease. Along with this, the brains of elderly healthy people were also examined.
The team found that neuroinflammation was more common in older people and was more pronounced in people with mild cognitive impairment and in people with dementia associated with Alzheimer’s.
Dew dispersion depends on microglia
Bioinformatics analysis has also confirmed that the proliferation of tau depends on the activation of microglia, a key element linking the effects of amyloid plaque aggregation with the proliferation of tau and ultimately with cognitive impairment and dementia.
Amyloid plaques don’t always lead to Alzheimer’s
“Many older people have amyloid plaques in their brains but never develop Alzheimer’s disease,” Dr. Pascal. It is known that a build-up of amyloid alone is not sufficient to cause dementia, and new results now suggest that “it is the interaction between neuroinflammation and amyloid pathology that triggers the proliferation of tau and ultimately brain damage.” and extends far beyond cognitive impairment.”
benefits of combination therapy
According to study author Dr. Based on the present study results, Tharrick Pascoll may also assume that a combination therapy, aimed at reducing the formation of amyloid plaques and attenuating neuroinflammation, may require separate treatment of the two pathologies. may be more effective than (As)
Author and source information
This text complies with the requirements of specialist medical literature, medical guidelines and current studies and has been checked by medical professionals.
- Tharik A. Pascoll, Andrea L. Benedet, Nicholas J. Ashton, Min Su Kang, Joseph Theriault, et al.: Microglial activation and tau jointly propagate in BRAK phases; In: Nature (veröffentlich 26.08.2021), Nature
- University of Pittsburgh School of Medicine: Brain Tissue Inflammation Drives Alzheimer’s Disease (veröffentlich 26.08.2021), University of Pittsburgh School of Medicine
This article is for general guidance only and is not to be used for self-diagnosis or self-treatment. He cannot take the place of visiting the doctor.
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