Tau reduction counteracts transcriptomic and behavioral abnormalities in an Alzheimer amyloid model

Differential effects of amyloid-β and tau on UCH gene expression in Drosophila models of Alzheimer's disease.

BACKGROUND Alzheimer's disease (AD) is a common neurodegenerative disorder characterized by progressive impairments in learning and memory. Substantial evidence indicates that dysfunction of the ubiquitin-proteasome system (UPS) in the AD brain leads to aberrant protein aggregation, ultimately resulting in synaptic dys...

Tau dysfunction in alzheimer’s disease: molecular and cellular mechanisms, genetic modulation, and therapeutic perspectives

Findings support a model in which tau dysfunction results from the convergence of molecular aberrations and genetic susceptibility within a pathological network involving amyloid-β, neuroinflammation, and synaptic failure.

Aberrant excitatory neuronal ERBB4 promotes Alzheimer’s disease pathology

It is demonstrated that, during AD progression in mice, astrocytes and microglia increase phagocytic elimination of excitatory synapses while reducing elimination of inhibitory synapses, suggesting that neuroinflammation alone may be dispensable for early AD synapse loss.

SorCS1 promotes synaptic and cognitive resilience despite amyloid pathology in Alzheimer’s disease model mice

A conserved serotonin receptor pathway is a druggable modifier of Tau pathology, neural circuit formation and neurodegeneration

A new Drosophila tauopathy model expressing eGFP-tagged human TauWT or the disease-associated TauP301L variant in the nervous system is established and 5-HT7R signaling is identified as a conserved and druggable modifier of Tau toxicity.

Comprehensive insights into Alzheimer's disease: Amyloid-β pathology, tau dysfunction, and neurodegenerative mechanisms.