In contrast, peptides deriving from microtubule-associated protein tau, presenilin 2 and serine/threonine-protein kinase TBK1 were exclusively reported to bind MHC molecules encoded by the HLA-DRB1 1501 allele, a recently-identified susceptibility gene for late onset Alzheimer's disease.
The majority of up-to-date epigenomic findings include reported modifications in the well-known LOAD core pathology loci MAPT, BACE1, APP (with FOS, EGR1), PSEN1, PSEN2, and highlight a central role of BDNF.
Identification of the key molecules involved in chronic copper exposure-aggravated memory impairment in transgenic mice of Alzheimer's disease using proteomic analysis.
We measured MAPT promoter methylation in a brain tissue cohort of early-onset Alzheimer's disease (EOAD) with defined causative mutations in the PSEN1 gene (Normal = 10, PSEN1 AD = 10), and idiopathic late-onset Alzheimer's disease (Normal = 12, LOAD = 12).
Late-onset Alzheimer's Disease (LOAD) is a common neurodegenerative disease [1], and the two well identified pathological hallmarks of LOAD are senile plaques formed from amyloid β peptides (Aβ) and neurofibrillary tangles (NFTs) consisting of hyperphorylated tau protein [2].
In addition, a synergistic effect of polymorphisms in ApoE ε4 and Tau gene STR loci rs5820604 (CA)(19) allele was found in the pathogenesis of AD (p = .025, OR [odds ratio] = 3.178, 95% CI [confidence interval] = 1.156-8.741).
To determine whether polymorphisms in the GSK3B gene and microtubule associated protein tau (MAPT) gene underpin susceptibility to late-onset Alzheimer's disease (LOAD), we conducted a case-control study in a Chinese cohort of 257 LOAD cases and 326 healthy controls matched for sex and age.