What’s happening in brain cells affected by Alzheimer’s disease?

Alzheimer’s disease, which affects more than 50 million people, is the most common form of dementia and occurs primarily in people over the age of 65. Tau protein. Tau protein stabilizes intracellular tube-like structures (microtubules) involved in the transport of nutrients within nerve cells. Beta amyloid is a protein present in the body that is formed by cleavage of amyloid precursor protein (APP).

APP is embedded in the cell membrane Nerve cell And it sticks out both inside and outside. It is typically cut once near the cell membrane. The inner part of the nerve cell is unstable and collapses. In patients with Alzheimer’s disease, two divisions occur, forming three parts. This new finding indicates that the inner part of nerve cells in patients with Alzheimer’s disease is more stable.It consists of only about 50 amino acid Under certain conditions Cell nucleus Along with other proteins such as FE65 and TIP60.this Protein complexAlso known as nuclear aggregates, it has the ability to manipulate gene expression in cells. “This suggests that aggregates are functioning in this area,” points out David Marks, lead author of RUB’s Cell Signaling group. More detailed analysis confirmed this evidence by finding proteins in the nuclear aggregates involved in DNA modification.

Two more protein candidates in the cell

“To better understand this mechanism, we look for other proteins that may be part of these aggregates and identify two more candidates involved in nuclear aggregates, the so-called tumor suppressor proteins P53 and PML. “We did,” explains David Marks. The research team found that nuclear aggregates formed from proteins APP-CT50, FE65, TIP60, and PML fuse with each other over time to produce larger nuclear aggregates. We have shown that we do this in experiments with living cells.

In addition, they examined aged brain samples and nerve tissue self-generated from induced pluripotent stem cells. “These mini-brain, so-called Brain organoidReflects the embryo and developmental stages of the brain fairly accurately, “explains Thorsten Müller. The research team found that relatively young brain organoids had few nuclear aggregates, but were older. Nuclear aggregates were present in the patient’s brain samples, which means that the process is age-dependent, “says Muller.

Stunning correlation

In addition, researchers have shown that for these brain samples, APP-CT50 and FE65 can form part of the so-called PML body that naturally occurs in many cell nuclei. Further analysis of hippocampal brain slices in patients with Alzheimer’s disease found that there was a significant correlation between the reduced number of PML bodies in the nucleus of areas of high beta-amyloid plaque load. Identified. In particular, such regions mean that there is higher expression and processing of APP. This may suggest that the translocation of APP-CT50 and FE65 to the nucleus is part of AD pathology and affects the fusion of PML bodies there.

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Nanoparticles help untangle amyloid beta plaque in Alzheimer’s disease

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For more information:
David Marks et al., Amyloid precursor protein enhances promyelocytic leukemia nucleolus fusion in the high plaque-loaded human hippocampal region. Acta Neuropathologica Communications (2021). DOI: 10.1186 / s40478-021-01174-x

Provided by
Ruhr University Bochum

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