Research Keyword: amyloid pathology

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

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.

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β-secretase inhibition prevents structural spine plasticity deficits in AppNL-G-F mice

Researchers tested whether a drug that blocks BACE1 (an enzyme involved in Alzheimer’s disease) could protect nerve cell connections in a mouse model of Alzheimer’s disease. They found that at high doses, the drug significantly improved the formation of new dendritic spines (connection points between neurons) and restored synaptic activity to near-normal levels. These findings suggest that using BACE1 inhibitors early in Alzheimer’s disease development, before widespread neuronal damage occurs, might help prevent cognitive decline.

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