Takashi Saito

Microglial AhR Drives Sex-Biased Amyloid Pathology

This study identifies microglial AhR as a regulator of sex-biased amyloid pathology, showing that AhR activation exacerbates amyloid deposition and that AhR deficiency reduces amyloid burden.

APPNL-F knock-in Alzheimer's Disease model mice reveal etiological convergence of aging and amyloidosis

This study characterizes the early stages of amyloidosis and neuroinflammation in APPNL-F AD model mice, revealing a link between microglial senescence and disease progression.

Selective agonism of GPR34 stimulates microglial uptake and clearance of amyloid β fibrils

This study identifies GPR34 as a regulator of microglial amyloid β fibril uptake, showing that its agonist enhances fibril clearance and that its expression declines with age and AD progression.

Misclassification in memory modification in AppNL-G-F knock-in mouse model of Alzheimers disease

This study uses computational modeling to show that AppNL-G-F mice exhibit misclassification in memory modification tasks due to altered internal states.

Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a knock in mouse model of Alzheimer's disease.

The paper shows that adenosine deficiency in a mouse model of Alzheimer's disease leads to synaptic hyperexcitability during the asymptomatic phase, which can be restored by pharmacologic or dietary interventions.