Fulin Ma

The paper shows that DNA damage increases with age and correlates with higher APP levels in Alzheimer's disease, suggesting DNA damage drives APP accumulation.

This study shows that APP overexpression and Aβ exposure affect neural activity differently in immature and mature cultures, suggesting distinct roles in Alzheimer's disease mechanisms.

The paper identifies TRIM47 as a genetic risk factor for white matter hyperintensity and shows it inhibits autophagy in brain endothelial cells.

The paper examines DNA damage and senescence in Alzheimer's disease cortex and finds they are increased and coupled in AD but not in controls.

This paper shows that full-length APP affects axon initial segment structure, linking APP function to Alzheimer's disease without relying on Aβ.