Publications by authors named "Karina S Vitanova"
Using spatial cell-type-enriched transcriptomics, we compare plaque-induced gene (PIG) expression in microglia-touching plaques, neighboring plaques, and far from plaques in an aged Alzheimer's mouse model with late plaque development. In 18-month-old APP knockin mice, with and without the Alzheimer's disease risk mutation Trem2, we report that expression of 38/55 PIGs have plaque-induced microglial upregulation, with a subset only upregulating in microglia directly contacting plaques. For seven PIGs, including Trem2, this upregulation is prevented in APPTrem2 mice.
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- Microglia play a critical role in Alzheimer's disease, particularly in their interaction with amyloid plaques and synaptic changes linked to amyloid beta, with novel findings from knock-in mice that avoid issues seen in transgenic models.
- In vitro experiments on genetically modified mice revealed that increased glutamate release occurs early, before plaque formation, but this response varies depending on the presence of plaques and age of the mouse.
- The study suggests that microglial activity impacts synaptic function, with partial microglial depletion mimicking aspects of the Alzheimer's phenotype, but overall changes in synaptic behavior occur late in disease progression and do not affect amyloid plaque levels.
Article Synopsis
- Dementia is the leading cause of death in the UK, responsible for over 12% of all deaths, and is becoming increasingly common globally as the population ages.
- The risk of developing dementia doubles every five years after age 65, making it urgent to find effective treatments to prevent a major health crisis.
- Recent research shifts focus towards the basal ganglia's role in dementia, suggesting that areas of the brain long thought unaffected in Alzheimer's may also be impacted, particularly in later disease stages.