Y and also visibly damaged subcortical areas [45,46]. Amyloid plaques in AD result from the deposition of amyloid beta (Ab) which is a putative pathogenic molecule in AD. Ab is the cleavage product of the amyloid precursor protein (APP) and APP mutations are associated with inherited forms of AD. The clinical implication or pathogenic consequences of brain amyloid deposition are still controversia
Y and also visibly damaged subcortical areas [45,46]. Amyloid plaques in AD result from the deposition of amyloid beta (Ab) which is a putative pathogenic molecule in AD. Ab is the cleavage product of the amyloid precursor protein (APP) and APP mutations are associated with inherited forms of AD. The clinical implication or pathogenic consequences of brain amyloid deposition are still controversia