Takaomi C. Saido

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.

The paper reports a cryo-EM structure of P301L/S320F double-mutant tau filaments induced in mice via peripheral AAV delivery, revealing a novel filament fold distinct from known tauopathies.

This study identifies CXCL10 as a driver of female-specific tau pathology progression in tauopathy model mice, revealing a sex-dependent mechanism independent of T cell or glial activation.

This study shows that expressing 3R tau isoforms in mice alters the disease course of traumatic brain injury, leading to different white matter damage and behavioral outcomes at subacute and chronic stages.

This study investigates how early binding of anti-amyloid antibodies to cerebral amyloid angiopathy (CAA) drives complement activation, inflammation, and ARIA in Alzheimer's disease mouse models.

This study compares the effects of TREM2 R47H mutation and TREM2 deficiency in aged AppNL-F mice, finding that the mutation causes mild, functionally distinct microglial changes compared to a null effect.

This study shows that Alzheimer's beta-amyloid pathology accelerates age-related hearing loss in a mouse model, with increased hearing thresholds, outer hair cell loss, and damage to the stria vascularis.

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.

This study uses mouse models with tau mutations to show two distinct pathogenic mechanisms in tauopathies, with different progression patterns and responses to amyloid.

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.

The paper shows that enhancing oligodendrocyte function in a mouse model of Alzheimer's Disease reduces neuronal damage and slows disease progression.

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.

This study shows that Alzheimer's disease mice exhibit age-dependent, odorant-specific changes in olfactory sensitivity, with hyperosmia to esters at 2 months and hyposmia at 4 months.

This study shows that APOE3 and APOE4 human astrocytes differentially affect Alzheimer's disease hallmarks in chimeric mice, with APOE3 reducing and APOE4 worsening pathology.

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 introduces a new mouse model, NLFTaum/h, that shows ageing and amyloid-β can initiate tau pathology without MAPT mutations, revealing interactions between age, Aβ, and human tau.

This study identifies early dysfunction of LEC-projecting dopamine neurons in AD mice, linking it to memory impairments and suggesting therapeutic potential through optogenetics or L-DOPA.

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.

The paper shows oligodendrocytes contribute to amyloid-β plaques in Alzheimer's disease, but neurons are required for plaque formation.

This study identifies Pla2g2f as a neuroprotective factor that maintains lipid homeostasis and mitigates aging-associated cognitive decline in a mouse model of Alzheimer's disease.

The paper uses CRISPR-Cas9 to edit the App gene in mice, reducing Alzheimer's disease symptoms and showing long-term benefits.

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.

This paper compares Aβ fibril structures in three mouse models of Alzheimer's disease, finding age-dependent differences in plaque morphology and polymorph maturation.

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.

The paper shows TSPO expression increases in activated microglia in rodent models but not in human neurodegenerative diseases, indicating species-specific differences in TSPO function.

This study shows that ageing-related myelin dysfunction drives amyloid-beta deposition in Alzheimer's disease mouse models, suggesting myelin integrity as an upstream risk factor.

This study examines network impairments in APPNL-G-F mice during sleep, finding NREM-specific changes in mPFC spindles and hippocampal SWRs linked to PV interneuron dysfunction.

This study shows that m6A accumulation correlates more strongly with MAPT pathology than beta-amyloid in an Alzheimer's mouse model.