Kanae Ando

The paper investigates the role of the 329HHK331 motif in Alzheimer's disease tau filament formation and shows that mutations in this region affect filament structure and seeding activity.

This study shows that nonfibrillar Aβ aggregates in APPE693Q mice disrupt presynaptic function without causing inflammation.

This study shows MARK2 in glial cells suppresses inflammation and reduces tau toxicity in neurodegenerative diseases.

This study shows MARK4 enhances stress granule formation and promotes tau accumulation through interactions with TIA1.

The paper shows that glucose uptake in pigment glia reduces inflammation and photoreceptor degeneration in a Drosophila model of tauopathy.

This study shows that increasing glucose uptake in Drosophila neurons improves ATP levels, reduces aging-related deficits, and extends lifespan, especially under dietary restriction.

This study shows that a MARK4 mutation linked to Alzheimer's disease increases tau phosphorylation and neurodegeneration through both direct and indirect mechanisms.

This study identifies molecular networks and key regulators in Alzheimer’s Disease using integrative genomics and experimental validation.