Article Abstract:
Alzheimer's disease is associated with cerebral amyloidosis and cerebral intraneuronal neurofibrillary pathology. A prominent feature of Alzheimer's disease is deposition of fibrils and plaques from amyloid protein in brain parenchyma and around vessels. Studies show that mutations of the Beta/A4 amyloid precursor protein (APP) gene promote amyloidogenesis. Transgenic animal models of cerebral amyloidosis are indispensable tools for research on the cellular pathobiology of amyloidogenesis, the pathogenesis of Alzheimer's disease and the treatment of amyloidosis and Alzheimer's dementia.
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Article Abstract:
A large part of chronic inflammatory disease research has been targeted at finding specific therapeutic strategies to break the cycle of cellular activation and tissue damage. Evidence indicates that apoptosis, or programmed physiological cell death, is a key check-point which controls the intensity of immune responses that may otherwise prove debilitating. Advances such as the use of Fas-induced death suggest possible resolution of chronic inflammation by therapeutic induction of apoptosis.
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Article Abstract:
Researchers have developed chemicals that mimic autoantigens that bind to MHC molecules and activate T cells. This could block the T-cell response to normal tissues, which leads to autoimmune disease.
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