Publications by authors named "Kirill Gorbachev"
Article Synopsis
- Excitotoxicity and tau-mediated toxicities are key factors in neuronal death related to Alzheimer's disease (AD), with issues like glutamate levels being critical.
- *The main glutamate transporter, EAAT2 (GLT-1), is deficient in AD brains, leading to cell death from excitotoxicity, while tau protein buildup correlates with cognitive decline.
- *Research using mouse models revealed that GLT-1 deficiency affects pathways linked to neuronal survival, while tau mutations disrupt endocytic pathways and mitochondria, highlighting potential therapeutic targets.*
Astrocyte-secreted glypican-4 drives APOE4-dependent tau hyperphosphorylation.
Proc Natl Acad Sci U S A
August 2022
Tau protein aggregates are a major driver of neurodegeneration and behavioral impairments in tauopathies, including in Alzheimer's disease (AD). Apolipoprotein E4 (), the highest genetic risk factor for late-onset AD, has been shown to exacerbate tau hyperphosphorylation in mouse models. However, the exact mechanisms through which APOE4 induces tau hyperphosphorylation remains unknown.
View Article and Find Full Text PDFAlzheimer's disease (AD) is the most frequent neurodegenerative disorder that commonly causes dementia in the elderly. Recent evidence indicates that network abnormalities, including hypersynchrony, altered oscillatory rhythmic activity, interneuron dysfunction, and synaptic depression, may be key mediators of cognitive decline in AD. In this review, we discuss characteristics of neuronal network excitability in AD, and the role of Aβ and tau in the induction of network hyperexcitability.
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