amyloid-beta – mycolab.ai

Microbial links to Alzheimer’s disease

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Researchers are investigating whether common infections from bacteria, viruses, and fungi might trigger or worsen Alzheimer’s disease. Studies show that pathogens like the bacteria that causes gum disease and certain herpes viruses can reach the brain and trigger inflammation and amyloid-beta accumulation, key features of Alzheimer’s. While the evidence is promising, scientists haven’t yet proven whether these infections cause Alzheimer’s or simply make existing disease worse.

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

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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.

Primary cilia in the mature brain: emerging roles in Alzheimer’s disease pathogenesis

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Primary cilia are small hair-like structures on brain cells that act like sensory antennas, helping regulate memory and thinking ability. In Alzheimer’s disease, these structures become abnormally shaped and function poorly, contributing to memory loss and cognitive decline. The shape and function of primary cilia change as the brain ages and when amyloid plaques develop, suggesting they could be targeted with new treatments to slow Alzheimer’s progression.

Research Topic: amyloid-beta

Microbial links to Alzheimer’s disease

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

Primary cilia in the mature brain: emerging roles in Alzheimer’s disease pathogenesis