Cláudia Guimas Almeida

This study shows CD2AP regulates dendritic spine morphology and synapse formation by modulating F-actin dynamics, linking its risk variants to Alzheimer's disease synaptic dysfunction.

The paper shows that ApoE4 increases Aβ42 levels in neurons and demonstrates intracellular intersection of ApoE with APP/Aβ in AD transgenic neurons.

The paper identifies deacidification of distal lysosomes in aged neurons as a mechanism driving synapse loss and shows that restoring acidification can reverse synaptic decline.

This study shows that Alzheimer's disease BIN1 coding variants increase intracellular Aβ by interfering with BACE1 recycling and early endosome enlargement.

The paper shows that neuronal aging increases beta-amyloid production through enhanced amyloid precursor protein endocytosis, contributing to synapse loss in aged neurons.