Background Chronic neuroinflammation, aggressive amyloid beta (Aβ) deposition, neuronal
cell loss, and cognitive impairment are pathological presentations of Alzheimer's disease …

Background An accumulating body of evidence is consistent with the hypothesis that
excessive or prolonged increases in proinflammatory cytokine production by activated glia is …

Background: P38 mitogen activated protein kinase (MAPK) α modulates microglia-mediated
inflammatory responses and a number of neuronal physiological processes. Objective: To …

Accumulating evidence indicates that p38 mitogen-activated protein kinase (MAPK) could
play more than one role in Alzheimer's disease (AD) pathophysiology and that patients …

P38 mitogen-activated protein kinase (MAPK) is a crucial target for chronic inflammatory
diseases. Alzheimer's disease (AD) is characterized by the presence of amyloid plaques …

Abstract Alzheimer's disease (AD), the most common cause of dementia in the elderly, is
pathologically characterized by extracellular deposition of amyloid‐β peptides (Aβ) and …

A myriad of environmental and genetic factors, as well as the physiologic process of aging,
contribute to Alzheimer's disease (AD) pathology. Neuroinflammation is and has been a …

Brain lesions in Alzheimer's disease (AD) include amyloid plaques made of Aβ peptides and
neurofibrillary tangles composed of hyperphosphorylated tau protein with synaptic and …

Background Hyperphosphorylation and aggregation of tau protein are the pathological
hallmarks of Alzheimer's disease and related tauopathies. We previously demonstrated that …

Targeted protein degradation (TPD) provides unique advantages over gene knockdown in
that it can induce selective degradation of disease-associated proteins attributed to …