"app cleavage and amyloid-beta degradation" has 4 results in Resources.

Amyloid-beta protein (A-beta) is the proposed causative agent of Alzheimer's disease (AD). One of the neuropathological hallmarks of AD is the accumulation of senile plaques in the brain. Senile plaques represent extracellular deposits of aggregated A-beta. Prior to its deposition as senile plaques, A-beta oligomerizes to exert pathological actions on neuron function and viability. AD therapies...

Sporadic, or late-onset, AD affects approximately 10% of the population over the age of sixty-five, making it the most prevalent neurodegenerative disorder. This devastating condition is characterized by progressive cognitive impairment and neurodegeneration, commencing in the hippocampus and cortex. Neuropathological hallmarks of AD include neuronal loss in the presence of neurofibrillary...

APP Cleavage & A-beta degradation Neuroscience research suggests a delicate balance between physiological and pathological events in the brain. Healthy neurons predominantly process beta-amyloid precursor protein (APP) via non-amyloidogenic alpha-secretase-driven cleavage. The majority of beta-amyloid peptide (A-beta) generated is rapidly degraded by a range of enzymes expressed in neurons and...

Alzheimer’s disease (AD) is a complex, neurodegenerative disorder that is characterized by neuroinflammation, neuronal cell death, the accumulation of amyloid plaques and neurofibrillary tangles (NFTs), and cortical and hippocampal atrophy. A key trigger of AD is believed to be the beta-Amyloid protein (A-beta), which is formed by the sequential enzymatic processing of Amyloid Precursor Protein...