familial Alzheimer’s disease

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.

New Positive TRPC6 Modulator Penetrates Blood–Brain Barrier, Eliminates Synaptic Deficiency and Restores Memory Deficit in 5xFAD Mice

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Researchers developed a new drug candidate called C20 that activates TRPC6 proteins in the brain. In studies with Alzheimer’s disease mouse models, C20 protected nerve connections from damage, restored memory function, and successfully crossed the blood-brain barrier. The compound shows promise as a potential treatment for Alzheimer’s disease by strengthening the connections between brain cells that are damaged in the disease.

Disease: familial Alzheimer's disease

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

New Positive TRPC6 Modulator Penetrates Blood–Brain Barrier, Eliminates Synaptic Deficiency and Restores Memory Deficit in 5xFAD Mice