抗TRPM2抗体，克隆9D8.1

Alzheimer’s Disease is a progressively deteriorating disease. It manifests itself with memory loss, confusion, problems with judgment, planning, concentration, and personality changes; and in it’s later stages, a decline in physical abilities. The disease’s causes, cures, and preventions are unknown; however, key proteins likely involved in the degenerative mechanism have been identified. Alzheimer’s Disease is characterized by neuronal loss, alterations in neurotransmitter systems, and the presence of neurofibrillary tangles composed of abnormally hyperphosphorylated tau proteins. A prominent feature of Alzheimer’s Disease is the formation of senile plaques in selected regions of the brain. The center of these plaques are composed mainly of fibrillary aggregates of a common, but not well understood, b amyloid peptides (Aβ). The Aβ peptides are generated from the larger amyloid-β precursor protein (APP) by the sequential action of β- and γ-secretase, and it is generally accepted that oligomeric forms of this Aβ are neurotoxic, resulting in disease progression.