Involvement of WAVE accumulation in Abeta/APP pathology-dependent tangle modification in Alzheimer's disease.

ABSTRACT: Synaptic deficits are closely correlated with cognitive dysfunction in Alzheimer's disease (AD), and synaptic integrity is regulated by the actin cytoskeleton. We demonstrated here that the Wiskott-Aldrich syndrome protein family verprolin-homologous protein (WAVE), a key molecule for actin assembly, co-aggregated with both hyperphosphorylated tau and phosphorylated collapsin response mediator protein 2 (CRMP2) in neurofibrillary tangles and abnormal neurites of the AD brain. Although phosphorylated CRMP2 accumulation was induced in the brains of JNPL3 mice, WAVE accumulation was not detected in the brains of either JNPL3 or Tg2576 mice that developed neurofibrillary tangles and amyloid-beta (Abeta) plaques, respectively. Interestingly, both phosphorylated CRMP2 accumulation and WAVE accum

SUBMITTER: Takata K 

PROVIDER: S-EPMC2708790 | biostudies-literature | 2009 Jul

REPOSITORIES: biostudies-literature