New Insights Into the Pathogenesis of Alzheimer's Disease

Abstract

Alzheimer's disease (AD), a common neurodegenerative disease in the elderly and the most prevalent cause of dementia, is characterized by progressive cognitive impairment. The prevalence of AD continues to increase worldwide, becoming a great healthcare challenge of the twenty-first century. In the more than 110 years since AD was discovered, many related pathogenic mechanisms have been proposed, and the most recognized hypotheses are the amyloid and tau hypotheses. However, almost all clinical trials targeting these mechanisms have not identified any effective methods to treat AD. Scientists are gradually moving away from the simple assumption, as proposed in the original amyloid hypothesis, to new theories of pathogenesis, including gamma oscillations, prion transmission, cerebral vasoconstriction, growth hormone secretagogue receptor 1α (GHSR1α)-mediated mechanism, and infection. To place these findings in context, we first reviewed the neuropathology of AD and further discussed new insights in the pathogenesis of AD.

Can the coronavirus infection penetrates the brain resulting in sudden anosmia followed by severe neurological disorders?

“…Alzheimer's disease (AD) is the most common type of neurodegenerative disorder for an old population mainly characterized by the presence of Aβ and tau protein particularly in the hippocampus and cerebral cortex. AD directly targets the CNS accompanied by severe neuroinflammation with the probability of being provoked by general systemic body injuries or infection [ 11 , 12 ]. Once senile plaques and neuroinflammatory tangles are deposited on different brain tissues and triggered by the exaggerated neural-immune system, a frequent disturbance in CNS homeostasis and gut type immune homeostasis is usually observed.…”

“…In AD patients, the imbalance between pro- and anti-inflammatory cytokines with more expression of M1 proinflammatory cytokines and chemokines could contribute to the progression of the AD stage. Previous studies have demonstrated that an exaggerated expression of IL-6, IFNγ, and TNF-α levels were observed in AD patient's resulting in dysregulation amyloid precursor protein (APP) along with synaptic and AD neuronal dysfunction [ 12 , 51 , 55 ].…”

Aluminium Binding to Modified Amyloid-β Peptides: Implications for Alzheimer’s Disease

“…The prevalence of Alzheimer’s disease (AD) continues to increase worldwide, becoming a great healthcare challenge of the twenty-first century [ 1 ]. AD is a progressive neurodegenerative disorder that gradually deprives the patient of cognitive function, being characterised by the presence of senile plaques and neurofibrillary tangles in the hippocampus and neocortex of the brain [ 2 ].…”

Hyperoside Protected Against Oxidative Stress-Induced Liver Injury via the PHLPP2-AKT-GSK-3β Signaling Pathway In Vivo and In Vitro

“…Oxidative stress contributes to the pathophysiological processes of alcoholic liver disease, non-alcoholic fatty liver disease, drug-induced liver disease, and other liver diseases by producing excessive reactive oxygen species (ROS), destroying mitochondrial structure and function, and reducing the level and activity of superoxide dismutase (SOD) and other cytoprotective proteins (Ivanov et al, 2017). Therefore, hepatic ROS is thought to be central in the pathogenesis of liver injury, and antioxidants including vitamin C and phenolic compounds have been extensively investigated to determine their ability to confer liver protection (Chougule and Kekunnaya, 2019;Fan et al, 2019;Su et al, 2019).…”