How is Alzheimer’s progressing?
The role that so-called neuroinflammation plays in the development of Alzheimer’s has been investigated in a recent study – with quite a surprising result. Neuroinflammation appears to be the main cause of the spread of pathologically misfolded proteins in the brain and the cause of the cognitive impairments in people with Alzheimer’s disease.
For the first time it has now been found in a study on living people that neuroinflammation – the activation of the immune cells located in the brain, which are known as microglial cells – is not just a consequence of the progression of Alzheimer’s. Rather, it is an important upstream mechanism that forms the basis for the development of the disease, report researchers from the University of Pittsburgh of their current study results. The study was published in the English-language journal “Nature Medicine“Published.
What happens in the brain in Alzheimer’s disease?
Alzheimer is 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 characteristic of Alzheimer’s disease are so-called tau tangles or deposits of tau protein, which form inside the nerve cells, according to the team.
Although studies on cultured cells and laboratory animals have already produced a lot of evidence that the activation of the microglia drives the spread 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
The results of the study suggest that targeted control of neuroinflammation is beneficial for people with early Alzheimer’s disease and can help reverse or at least slow down the accumulation of pathological tau protein in the brain and prevent dementia, the experts report in a 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 the disordered knots of tau protein fibers and amyloid plaques spread in the brain and lead to dementia, the experts used live imaging to examine the brains of people who are already at various stages Alzheimer’s disease. In addition, 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 impairments and those with Alzheimer’s-associated dementia.
Spread of dew depends on microglia
Bioinformatics analyzes have also confirmed that the spread of tau depends on the activation of the microglia, a key element that links the effects of amyloid plaque aggregation with the spread 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,” explains Dr. Pascoal. It is known that amyloid build-up alone is not enough to cause dementia, and the new results now suggest “that it is the interaction between neuroinflammation and amyloid pathology that triggers the spread of tau and eventually spreads too far Brain damage and cognitive impairment. “
Advantages of combination therapy
According to study author Dr. On the basis of current study results, Tharick Pascoal can also assume that a combination therapy, which aims to reduce the formation of amyloid plaques and contain neuroinflammation, could be more effective than the separate treatment of both pathologies. (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.
- Tharick A. Pascoal, Andrea L. Benedet, Nicholas J. Ashton, Min Su Kang, Joseph Therriault, et al.: Microglial activation and tau propagate jointly across Braak stages; in: Nature (veröffentlicht 26.08.2021), Nature
- University of Pittsburgh School of Medicine: Brain Tissue Inflammation Drives Alzheimer’s Disease (veröffentlicht 26.08.2021), University of Pittsburgh School of Medicine
This article is for general guidance only and is not intended to be used for self-diagnosis or self-treatment. He can not substitute a visit at the doctor.