Novel Mechanism Involving Beta-Amyloid Protein Linked to Alzheimer’s Disease

Novel Mechanism Involving Beta-Amyloid Protein Linked to Alzheimer’s Disease
An international team led by researchers at The Rockefeller University and Columbia University recently published in the journal Nature Medicine a novel mechanism through which it is possible to decrease the production of beta-amyloid protein, a key factor in Alzheimer’s disease development. The study is entitled “APP intracellular domain–WAVE1 pathway reduces amyloid-β production”. Alzheimer’s disease is a neurodegenerative disorder characterized by cognitive and behavioral problems. It is the most common form of dementia in the elderly with patients initially experiencing memory loss and confusion that gradually leads to behavior and personality changes, a decline in cognitive abilities and ultimately to severe loss of mental function. Alzheimer’s disease is characterized by the loss of neurons responsible for memory and learning, and brain formation of amyloid plaques containing aggregates of sticky beta-amyloid proteins. It is estimated that 44 million people worldwide suffer from Alzheimer's or other form of dementia. In the study, researchers investigated in more detail the pathways that lead to the generation and accumulation of beta-amyloid proteins. The team found that the molecule that originates beta-amyloid, the amyloid precursor protein (APP), more exactly the intracellular domain of the protein (AICD), can downregulate the expression of a protein called WAVE1 in neuron cells, thereby limiting the pr
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