© Patricio Opazo/Daniel Choquet/IINS Rat hippocampal neurons in primary culture, showing a fluorescent soluble protein (left) and trajectories corresponding to the movement of the glutamate receptors on its surface, measured by following individual molecules.
The accumulation of amyloid peptides in the form of plaques in the brain is one of the primary indicators of Alzheimer's disease. While the harmful effects of amyloid peptide aggregates are well established, the mechanism through which they act on brain cells remains ill-defined. Researchers from CNRS and université de Bordeaux have just revealed that they alter the usual functioning of connections between neurons by interacting with a key enzyme of synaptic plasticity. The results will be published on June 12, 2018 in the journal Cell Reports . Alzheimer's disease, which affects nearly a million French people, is characterized by a premature alteration of the patient's cognitive faculties, followed by neuronal degeneration in late stages. Three types of brain lesions are characteristic of the illness: neuronal loss, fibrillar degeneration, and the accumulation of amyloid peptides that form on amyloid plaques. The respective involvement of these different elements in developing the symptoms of the illness is still poorly understood.
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