Yasuo Ihara

Curcumin improves tau-induced neuronal dysfunction of nematodes.

[Overview on Alzheimer's disease].

GAB2 is not associated with late-onset Alzheimer's disease in Japanese.

gamma-Secretase: successive tripeptide and tetrapeptide release from the transmembrane domain of beta-carboxyl terminal fragment.

Central nervous system-specific deletion of transcription factor Nrf1 causes progressive motor neuronal dysfunction.

The ubiquitin-proteasome system and the autophagic-lysosomal system in Alzheimer disease.

Suspected limited efficacy of γ-secretase modulators.

SORL1 is genetically associated with late-onset Alzheimer's disease in Japanese, Koreans and Caucasians.

Modulation of lipid kinase PI4KIIα activity and lipid raft association of presenilin 1 underlies γ-secretase inhibition by ginsenoside (20S)-Rg3.

Substrate ectodomain is critical for substrate preference and inhibition of γ-secretase.

γ-Secretase associated with lipid rafts: multiple interactive pathways in the stepwise processing of β-carboxyl-terminal fragment.

The homologous carboxyl-terminal domains of microtubule-associated protein 2 and TAU induce neuronal dysfunction and have differential fates in the evolution of neurofibrillary tangles.

Lack of genetic association between TREM2 and late-onset Alzheimer's disease in a Japanese population.

Immunostaining of oxidized DJ-1 in human and mouse brains.

Identification of key amino acids responsible for the distinct aggregation properties of microtubule-associated protein 2 and tau.

The A673T mutation in the amyloid precursor protein reduces the production of β-amyloid protein from its β-carboxyl terminal fragment in cells.

Toxic tau oligomer formation blocked by capping of cysteine residues with 1,2-dihydroxybenzene groups.

Alanine substitutions in the GXXXG motif alter C99 cleavage by γ-secretase but not its dimerization.

Semagacestat Is a Pseudo-Inhibitor of γ-Secretase.

Distinct deposition of amyloid-β species in brains with Alzheimer's disease pathology visualized with MALDI imaging mass spectrometry.

Imbalanced Expression of Tau and Tubulin Induces Neuronal Dysfunction in Models of Tauopathy.