Long-term effects of amyloid targeted therapy can be studied using a mechanistic translational model of amyloid beta (Aβ) distribution and aggregation calibrated on published data in mouse and human species. Alzheimer disease (AD) pathology is modeled utilizing age-dependent pathological evolution for rate constants and several variants of explicit functions for Aβ toxicity influencing cognitiv...

alzheimer’s disease (ad) is a uniquely human disorder. although the pathogenesis of ad is not fully understood, growing evidence indicates that the deposition of beta-amyloid (aβ) and the local reactions of various cell types to this protein play major roles in the development of the disease. in the present study transgenic mice expressing mutant amyloid precursor protein (app) has been used. t...

Abstract Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Amyloid-beta (Aβ) deposition, one processes involved in pathophysiology AD, has inspired interest targeted therapies, including monoclonal antibodies. Aducanumab acts as a fully human IgG1 antibody against Aβ by binding to amyloid plaques and was approved Food Drug Administration (FDA) first disease-modifying drug for...

Alzheimer’s disease (AD) is a neuropathology characterized by progressive cognitive impairment and dementia. The attributed to senile plaques, which are aggregates of amyloid beta (Aβ) outside nerve cells; neurofibrillary tangles, filamentous accumulations phosphorylated tau in loss neurons the brain tissue. Immunization an AD mouse model with Aβ-eliminated pre-existing plaque amyloids prevente...

different treatment strategies of alzheimer's disease (ad) are being studied for treating or slowing the progression of ad. many pharmaceutically important regulation systems operate through proteins as drug targets. here, we investigate the drug target proteins in beta-amyloid (aβ) injected rat hippocampus treated with lavandula angustifolia (la) by proteomics techniques. the reported stu...

Alzheimer's disease (AD) is poised to become the most serious healthcare issue of our generation. The leading theory of AD pathophysiology is the Amyloid Cascade Hypothesis, and clinical trials are now proceeding based on this hypothesis. Here, we review the original evidence for the Amyloid Hypothesis, which was originally focused on the extracellular deposition of beta amyloid peptides (Aβ) i...

Alzheimer's disease is a neurodegenerative condition characterized by an accumulation of toxic amyloid beta- (Aβ-)peptides in the brain causing progressive neuronal death. Aβ-peptides are produced by aspartyl proteinase-mediated cleavage of the larger amyloid precursor protein (APP). In contrast to this detrimental "amyloidogenic" form of proteolysis, a range of zinc metalloproteinases can proc...

Extracellular accumulation of amyloid beta protein (Aβ) plays a central role in Alzheimer's disease (AD). Some metals, such as copper, lead, and aluminum can affect the Aβ accumulation in the brain. However, the effect of mercury on Aβ accumulation in the brain is not clear. Thus, this study was proposed to estimate whether mercury concentration affects Aβ accumulation in PC12 cells. We treated...

The amyloid hypothesis has driven drug development strategies for Alzheimer's disease for over 20 years. We review why accumulation of amyloid-beta (Aβ) oligomers is generally considered causal for synaptic loss and neurodegeneration in AD. We elaborate on and update arguments for and against the amyloid hypothesis with new data and interpretations, and consider why the amyloid hypothesis may b...

By maintaining the Na(+) and K(+) transmembrane gradient mammalian Na,K-ATPase acts as a key regulator of neuronal electrotonic properties. Na,K-ATPase has an important role in synaptic transmission and memory formation. Accumulation of beta-amyloid (Aβ) at the early stages of Alzheimer's disease is accompanied by reduction of Na,K-ATPase functional activity. The molecular mechanism behind this...