synaptic dysfunction

N6-methyladenosine-modified circRIMS2 mediates synaptic and memory impairments by activating GluN2B ubiquitination in Alzheimer’s disease

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This research reveals how an abnormal RNA molecule called circRIMS2 contributes to Alzheimer’s disease by damaging brain synapses and impairing memory. Scientists found that circRIMS2 levels are elevated through a chemical modification called m6A methylation, and this causes a cascade of events leading to the destruction of important proteins needed for brain communication. The study shows that blocking this damaging pathway using a specially designed peptide can restore memory and synaptic function in Alzheimer’s disease models, offering hope for new therapeutic approaches.

Long term worsening of amyloid pathology, cerebral function, and cognition after a single inoculation of beta-amyloid seeds with Osaka mutation

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Researchers found that a single exposure to mutated amyloid-beta proteins (Aβ Osaka) in the brains of genetically modified mice caused lasting damage over four months. The mutated proteins triggered more severe memory loss, brain connectivity problems, and synapse damage compared to normal amyloid-beta. This suggests that even one encounter with mutated amyloid proteins can set off a chain reaction of disease progression that persists long after initial exposure.

The regulatory variant rs1950834 confers the risk of depressive disorder by reducing LRFN5 expression

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Researchers identified a genetic variant (rs1950834) that increases depression risk by reducing production of LRFN5, a protein important for brain connections. They found this variant affects how brain cells in a region called the nucleus accumbens produce LRFN5. When LRFN5 levels are low, mice become more depressed and sensitive to stress, but boosting LRFN5 protects against depression. This discovery could lead to new ways to diagnose and treat depression.

Research Keyword: synaptic dysfunction

N6-methyladenosine-modified circRIMS2 mediates synaptic and memory impairments by activating GluN2B ubiquitination in Alzheimer’s disease

Long term worsening of amyloid pathology, cerebral function, and cognition after a single inoculation of beta-amyloid seeds with Osaka mutation

The regulatory variant rs1950834 confers the risk of depressive disorder by reducing LRFN5 expression