Taken together, such abnormalities in endosomal trafficking may render the glutamate synapse more vulnerable and less responsive to stimuli by promoting the intracellular accumulation of AMPA receptors, a mechanism that closely resembles the impaired endosomal-induced aberrant intracellular accumulation of neurofibrillary tangles of hyper-phosphorylated tau and amyloid-b plaques in Alzheimer’s disease [80] and a-synuclein in Parkinson’s disease [81]. This evidence concerns the gene MAPT and Alzheimer disease.