Chemical Compound Can Restore Neural Function in Familial Alzheimer’s, Study Finds

Chemical Compound Can Restore Neural Function in Familial Alzheimer’s, Study Finds
  A mutation in a gene linked to familial Alzheimer’s disease promotes the disease by reducing the points of contact between nerve cells and impairing neuronal communication, a study has found. A chemical compound, called EVP4593, partially rescued the mutation's negative effects, suggesting it may hold a potential therapeutic role for familial Alzheimer's. The study, “Antagonist of neuronal store-operated calcium entry exerts beneficial effects in neurons expressing PSEN1ΔE9 mutant linked to familial Alzheimer disease” was published in the journal Neuroscience. Mutations in the amyloid precursor protein (APP) and presenilin (PS1 and PS2) genes cause an inherited form of Alzheimer’s disease, or familial Alzheimer's. Most familial Alzheimer's cases are caused by mutations in the PS1 gene, which codes for a protein called presenilin. This protein belongs to a complex of molecules that splits amyloid precursor protein to produce beta amyloid, whose toxic aggregates are thought to be at the center of the toxic protein clumps and neuroinflammation that drive Alzheimer’s. Now, a team of researchers at Russia's Peter the Great St. Petersburg Polytechnic University (SPbPU) investigated a mutation in the PS1 gene, called PSEN1ΔE9, found in a group of familial Alzheimer's patients in Finland. The researchers investigated how the mutation, which removes a part of the PS1 gene, affected disease progression. They began by introducing t
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