Amyloid β (Aβ) refers to peptides derived from Amyloid precursor protein that vary in length from 36-43 amino acids. Aβ(s) peptides, their peptide fragments and mutated fragments are used to study a wide range of metabolic and regulatory functions including activation of kinases, regulation of cholesterol transport, function as a transcription factor, and regulators of inflammation. Aβ(s) peptides and their peptide fragments are also used to study oxidative stress, metal binding and mechanisms of protein cross-linking in the context of diseases such as Alzheimer′s disease and neurodegeneration.
Neurobiology of learning and memory, 123, 168-178 (2015-06-14)
Single-session anodal transcranial direct current stimulation (tDCS) can improve the learning-memory function of patients with Alzheimer's disease (AD). After-effects of tDCS can be more significant if the stimulation is repeated regularly in a period. Here the behavioral and the histologic
Neurobiology of learning and memory, 95(3), 270-276 (2010-12-15)
Alzheimer's disease (AD) is a debilitating neurodegenerative disorder characterized by increased β-amyloid (Aβ) deposition and neuronal dysfunction leading to impaired learning and recall. Ageing, heredity, and induced oxidative stress are among proposed risk factors. The increased frequency of the disease
The journal of physical chemistry. B, 114(34), 11261-11271 (2010-08-10)
There is no consensus on the coordinating ligands for Cu(2+) by Abeta. However, the differences in peptide sequence between human and rat have been hypothesized to alter metal ion binding in a manner that alters Cu(2+)-induced aggregation of Abeta. Herein
Neurobiology of aging, 29(12), 1805-1814 (2007-06-16)
Although numerous inflammation pathways have been implicated in Alzheimer's disease, the involvement of the kallikrein-kinin system is still under investigation. We anatomically localized and quantified the density of kinin B(1) and B(2) receptors binding sites in the rat brain after
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the accumulation of β-sheet-rich amyloid oligomers or fibrils which are associated with cellular toxicity in the brain. Inhibition of Aβ aggregation could be a viable therapeutic strategy for slowing and/or
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