Scientists have been studying the biological origin of Alzheimer’s disease for years. Although the various risk factors are well known, the exact origin of the onset of brain degeneration has not yet been formally established. The avenue most seriously considered is that of the appearance of amyloid plaques outside the neurons of the brain, preventing it from functioning properly, but no treatment preventing the formation of this “amyloid cascade” seems to work.
A new study, published on June 2 in the journal nature neuroscience, challenges this assumption. According to researchers at the Nathan Kline Institute’s Dementia Research Center (USA), the disease process starts inside neurons and not outside and the appearance of amyloid plaques would be a consequence and not a cause of the disease.
An alternative origin of amyloid plaques
“To identify dysfunctions in lysosomes, that small part of the neuron that is used to ‘digest’ useless or degraded components, we crossed mice that develop early- or late-onset Alzheimer’s disease pathology. In the five models of mice studied, we have demonstrated early deficiencies in neuronal activity long before extracellular deposition of β-amyloid”, the researchers point out.
This discovery will not revolutionize research on the disease. But it opens the way to new hypotheses and in particular that according to which there would be several Alzheimer’s diseases, of more or less precocious form and of different evolution.
“This new evidence changes our fundamental understanding of Alzheimer’s disease progression. It also explains why so many experimental therapies designed to remove amyloid plaques have failed to arrest disease progression because brain cells are already paralyzed before the plaques form completely outside the cell”, say the researchers
Source : Faulty autolysosome acidification in Alzheimer’s disease mouse models induces autophagic build-up of Aβ in neurons, yielding senile plaquesNature Neuroscience, June 2022
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