The major pathological hallmarks in the brain of AD patients are neuronal loss, synaptic dysfunction, and plaque deposition, which primarily consists of Amyloid-Î² (AÎ²) peptide and neurofibrillary tangles (NFTâs) composed of phosphorylated tau protein. AÎ² aggregation is widely regarded as the chief component in the pathogenesis of AD. AÎ² deposition primarily occurs in cortical regions responsible for memory and learning as well as in the small blood vessels of the meninges and cerebral cortex. Oxidative stress and mitochondrial dysfunction are also key contributors to the pathological cascade leading to AD. Researchers have attempted to delineate the biological processes by which the neuropathology following TBI may elicit a pathogenic cascade contributing to the progression of AD and other NDs.
A journal is a periodical publication intended to further progress of science, usually by reporting new research. Most journals are highly specialized, although some of the oldest journals publish articles, reviews, editorials, short communications, letters, and scientific papers across a wide range of scientific fields. Journals contain articles that peer reviewed, in an attempt to ensure that articles meet the journal's standards of quality, and scientific validity. Each such journal article becomes part of the permanent scientific record.
Last date updated on September, 2014