Alzheimer’s: cause of disease progression discovered in the brain

Causes of Alzheimer’s Disease Progress identified

For the first time, a research team was able to show how Alzheimer’s disease spreads in the brain. The working group found that the degenerative disease “develops very differently than previously assumed”. According to this, several sources of harmful deposits in the brain are responsible for the course of the disease.

Researchers at the University of Cambridge showed for the first time that Alzheimer’s disease spreads in the brain in a completely different way than previously thought. Local proliferation of protein deposits, which increase slowly but exponentially in several foci of the disease at the same time, are responsible for the progression of the disease, according to the study. The research results were recently published in the renowned specialist journal “Science Advances“Published.

Alzheimer’s breaks out in several regions of the brain at the same time

Up until now, it was mostly assumed that Alzheimer’s disease starts from a point in the brain and then sets off a chain reaction that ultimately leads to the death of brain cells. However, the current study results paint a different picture. Apparently, the neurodegenerative disease begins early in several regions of the brain at the same time through the accumulation of so-called tau fibrils and amyloid plaque.

According to the researchers, these harmful deposits multiply slowly, but at an exponential rate. This process explains why the disease begins with mild cognitive impairment and then slowly but steadily worsens until death occurs in the terminal stages. For the first time, the working group developed a model that depicts the course of the disease.

The course of the disease is comprehensively documented

The international team is evaluating brain samples from deceased Alzheimer’s patients. In addition, the researchers carried out brain scans (PET) on living people with Alzheimer’s disease at various stages of the disease – from mild cognitive disorders to the later stages with severe clumping in the brain.

Two key proteins allow the disease to progress

It was previously known that disease progression was linked to two key proteins. In the course of the disease, proteins of the type tau and amyloid-beta increasingly accumulate in the brain and form plaques and clumps that limit the function of the brain. Such deposits are referred to in medicine as Alzheimer’s aggregates.

As a result of the accumulation, brain cells die and the brain begins to shrink. This manifests itself in those affected by memory loss, personality changes and difficulties in performing everyday tasks.

The course of the disease could be mapped for the first time

With the data collected in the various stages of the disease and a mathematical model, the researchers have succeeded in mapping the mechanism that controls the progression of Alzheimer’s disease. It was revealed for the first time that the disease does not spread from one brain region to the other, as is generally assumed, but rather grows in several brain regions at the same time.

The findings expand our understanding of Alzheimer’s disease and other neurodegenerative diseases. At the same time, research opens up new approaches for possible treatments.

On the wrong track

According to the research team, Alzheimer’s disease has been described as a chain reaction or cascade in the brain for many years. Since the disease spreads slowly over many decades and it has only recently been possible to identify those affected in the early stages, an investigation of the course of the disease from the beginning to the end stage has so far only been possible to a limited extent. In addition, many research results have been based predominantly on animal models.

Possible reason for previous treatment approaches failing

“Until now it was thought that Alzheimer’s developed in a similar way to many types of cancer: the aggregates form in a region and then spread in the brain,” explains lead author Dr. Georg Meisl from the University of Cambridge. “Instead, we found that by the time Alzheimer’s disease started, aggregates were already present in multiple regions of the brain, so trying to stop the spread between regions would hardly slow the disease down.”

Paradigm Shift in Alzheimer’s Disease

According to the working group, it is the first time that data collected from humans has been used to track which processes are driving the development of Alzheimer’s disease. “This research shows how valuable it is to work with human data instead of imperfect animal models,” emphasizes Professor Tuomas Knowles from the research group. The present results are an important step on the way to a functioning therapy.

Point of attack discovered

The research results also draw attention to a possible point of attack. Because the replication of tau aggregates is surprisingly slow. “Neurons are very good at preventing aggregates from forming, but we need to find ways to make them even better if we are to develop an effective treatment,” summarizes Professor Sir David Klenerman, who works at the University’s UK Dementia Research Institute of Cambridge operates. (vb)

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.

Author:

Diploma-Editor (FH) Volker Blasek

Sources:

  • University of Cambridge: Scientists identify the cause of Alzheimer’s progression in the brain (veröffentlicht: 29.10.2021), cam.ac.uk
  • Deutsches Ärzteblatt: How Alzheimer’s Disease Spreads in the Brain (published: November 1, 2021), aerzteblatt.de
  • Georg Meisl et al. ‘In vivo rate-determining steps of tau seed accumulation in Alzheimer’s disease.’ Science Advances (2021). DOI: 10.1126/sciadv.abh1448, science.org

Important NOTE:
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.

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Alzheimer’s: cause of disease progression discovered in the brain

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