Hiroki Sasaguri

The paper shows that inducing a hibernation-like brain state in AD mice slows amyloid plaque accumulation and reduces neuroinflammation without targeting specific pathways.

This study investigates the effect of orexin receptor antagonists on early-stage Alzheimer's disease in mice, finding they prevent cognitive impairment and amyloid-beta accumulation.

The paper compares synaptic kinetics across mammals and finds human neurons have faster excitatory transmission, leading to better pattern detection in noise during unsupervised learning.

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

The paper describes the development of triple MAPT mutation knock-in mice that exhibit early tau pathology and behavioral abnormalities, useful for studying frontotemporal dementia and related tauopathies.

This paper investigates the metabolic stability and deposition of A{beta}3pE-42, a target of the Alzheimer's antibody donanemab, showing it is more stable than other A{beta}X-42 species and accumulates with age.

This study investigates the sex-specific role of Cst7 in microglia in an amyloid-driven Alzheimer's Disease model, finding sexually dimorphic effects on endolysosomal function and inflammation.

This paper introduces an automated AI-driven system for continuous phenotyping of mouse cognition and behaviour, showing it can distinguish hippocampal and Alzheimer's models better than standard tests.

This study compares the roles of NEP and IDE in Aβ metabolism using double knockout mice, finding NEP primarily degrades insoluble Aβ and its deficiency contributes to AD pathology.

This study develops App knock-in mice without Swedish mutations to investigate β-secretase inhibition and endosomal abnormalities in Alzheimer's disease.

This paper introduces a new mouse model that accumulates wild-type human Aβ rapidly, showing more severe cored plaque pathology and neuroinflammation than existing models.

This study identifies α-endosulfine as a negative regulator of neprilysin activity, showing that its deficiency reduces amyloid β42 deposition in Alzheimer's disease models.

This paper describes the creation of the first non-human primate model of familial Alzheimer's disease using genome editing to introduce a PSEN1 mutation associated with early-onset AD.

This study identifies SST1 and SST4 as redundant regulators of neprilysin, a key amyloid beta-degrading enzyme, and shows that targeting these receptors reduces Aβ pathology and improves cognition in an AD mouse model.