Recent Progress in Alzheimer’s Disease Research, Part 1: Pathology

Abstract

The field of Alzheimer's disease (AD) research has grown exponentially over the past few decades, especially since the isolation and identification of amyloid-β from postmortem examination of the brains of AD patients. Recently, the Journal of Alzheimer's Disease (JAD) put forth approximately 300 research reports which were deemed to be the most influential research reports in the field of AD since 2010. JAD readers were asked to vote on these most influential reports. In this 3-part review, we review the results of the 300 most influential AD research reports to provide JAD readers with a readily accessible, yet comprehensive review of the state of contemporary research. Notably, this multi-part review identifies the "hottest" fields of AD research providing guidance for both senior investigators as well as investigators new to the field on what is the most pressing fields within AD research. Part 1 of this review covers pathogenesis, both on a molecular and macro scale. Part 2 review genetics and epidemiology, and part 3 covers diagnosis and treatment. This part of the review, pathology, reviews amyloid-β, tau, prions, brain structure, and functional changes with AD and the neuroimmune response of AD.

Preventive Electroacupuncture Ameliorates D‐Galactose‐Induced Alzheimer’s Disease‐Like Pathology and Memory Deficits Probably via Inhibition of GSK3β/mTOR Signaling Pathway

“…Extracellular Aβ plaques and intracellular neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau proteins in the cerebral cortex and hippocampus are the typical pathological changes of AD [2,7]. It is well recognized that the severity of dementia is strongly correlated with NFTs rather than senile plaques [8,9].…”

Phosphorylation Signaling in APP Processing in Alzheimer’s Disease

“…There are two typical pathological hallmarks in AD: the accumulation of amyloid plaques consisting of amyloid-β (Aβ) proteins in the brain parenchyma of AD patients and the formation of neurofibrillary tangles composed of hyperphosphorylated tau filaments [6]. Additional pathological changes in AD include the presence of chronic neuroinflammation, gradual neuronal loss and synaptic dysfunction, and impairments in the blood-brain barrier (BBB) [7]. Age is the biggest nongenetic risk factor for AD, as revealed by the exponential increase in the incidence of AD with the advancement of age [2].…”

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

“…It is well known that AD is a chronic and progressive neurodegenerative disease, with gradual memory loss as the main clinical syndrome. In the general pathology, there is nervous tissue atrophy, neuron and synapse loss, as well as neuronal subcellular structure and function disorders, which are all involved in the development and clinical manifestation of AD 1 2 . It is reported that when animals were intracerebroventricularly injected with Aβ, some neurotoxic events occur in the brain involving neuron loss, calcium homeostasis disruption, neuron apoptosis, and reactive oxygen species overproduction 3 .…”