Takahisa Kanekiyo

The paper identifies W2A-28, a dual modulator of class I HDACs and Wnt/β-catenin signaling, as a potential therapeutic for Alzheimer's disease.

This paper describes the discovery and validation of C273, a mitochondrial complex I modulator that reduces Alzheimer's disease pathology by enhancing cellular resilience through AMPK-mediated pathways.

The paper identifies epigenetic changes in Alzheimer's disease brains linked to tau pathology, highlighting oligodendrocyte gene perturbations as a potential common mechanism across tauopathies.

The paper assesses a novel mitochondrial complex I inhibitor, C458, in vitro and in vivo, showing it protects against Aβ toxicity, improves brain energetics, and reduces inflammation in Alzheimer's disease models.

This study examines how APOE genotypes affect brain metabolome changes with aging in mice, finding that APOE2 genotype is associated with better mitochondrial function and BCAA utilization.

This study uses human brain organoid microphysiological systems to show that AD patient monocytes cause increased inflammation and reduced Aβ clearance in organoids compared to controls.

This study examines PINK1-PRKN signaling in mice during aging, showing increased gene expression and enzymatic activity in multiple tissues, with the heart showing the most pronounced activation.

This study identifies ABCA7-dependent neuropeptide Y signaling as a resilience mechanism critical for synaptic integrity and its disruption as a risk factor for Alzheimer's disease.

This study performs a genome-wide association study of brain biochemical phenotypes in Alzheimer's patients, identifying novel genetic loci and highlighting distinct genetic architectures for AD-related proteins.

The paper shows that partial inhibition of mitochondrial complex I protects against neurodegeneration in Alzheimer's mice by improving energy homeostasis, synaptic function, and reducing inflammation.

This study shows that inhibiting mitochondrial complex I with CP2 reduces pTau levels and improves cognitive and metabolic function in 3xTg-AD mice.

This study shows APOE2 is linked to longer lifespan regardless of Alzheimer's disease, with preserved activity and lipid metabolism playing a role.