Elsevier

Neurobiology of Aging

Volume 13, Issue 5, September–October 1992, Pages 617-621
Neurobiology of Aging

Commentary
β-Amyloid precursor protein and alzheimer's disease: The peptide plot thickens

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Cited by (57)

  • Truncation and activation of dual specificity tyrosine phosphorylation-regulated kinase 1AbyCalpain I: A molecular mechanism linked to Tau pathology in Alzheimer disease

    2015, Journal of Biological Chemistry
    Citation Excerpt :

    Truncated Dyrk1A forms in AD brain could not be immunodepleted by anti-His antibody and were around 40–50 kDa, indicating that they were similar to the truncated Dyrk1A forms produced by calpain I in vitro and that the truncation was located upstream of the His repeat. Many putative etiologic factors of AD, including excitotoxicity, β-amyloid neurotoxicity, and free radical injury, have in common the potential for disrupting intracellular calcium homeostasis (75–77). Although there is a lack of direct evidence of altered calcium homeostasis in AD brain, dysregulation of calcium is one of the major hypotheses that may explain the pathogenic mechanism of the disease (59, 78).

  • Okadaic acid-induced Tau phosphorylation in rat brain: Role of NMDA receptor

    2013, Neuroscience
    Citation Excerpt :

    It seems that OKA (ICV) activates a link involving the calcium regulating genes calpain and CaMKII, and the neurodegeneration-associated gene Tau, which may be associated with memory dysfunction and neurotoxicity. Intracellular Ca2+ alteration is a major contributory factor for neuronal excitotoxicity seen in AD (Mattson and Rydel, 1992). Activation of glutamate receptors is believed to play a major role in the neuronal cell death (Mattson, 1996).

  • The effects of lignan-riched extract of Shisandra chinensis on amyloid-β-induced cognitive impairment and neurotoxicity in the cortex and hippocampus of mouse

    2013, Journal of Ethnopharmacology
    Citation Excerpt :

    The Roles of Aβ in the neuronal degeneration of AD have been suggested based on experimental results obtained in rodent studies. In particular, the synthetic Aβ seemed to be responsible for neurotoxic and oxidative events leading to neurodegenerative damage in hippocampal neurons or the cultured cortical neurons (Yankner et al., 1990; Mattson and Rydel, 1992; Takashima et al., 1993). Animal experiments showed the evidences that the accumulation of Aβ is closely correlated with cognitive impairment found in AD patients.

  • Immunomodulatory and therapeutic activity of curcumin

    2011, International Immunopharmacology
    Citation Excerpt :

    One of the possible mechanisms suggested in curcumin's ability to inhibit plaque formation is the high affinity with which it binds redox reactive metals such as copper and iron and therefore may act as a potent anti-oxidant by chelating redox reactive metals [137]. Amyloid plaque burden has been associated with depolarizing of the neuronal membrane and enhanced glutamate-mediated excitotoxicity [138,139] that results in impaired electrical firing of the neurons. Curcumin administration has been shown to prevent misfiring of neurons following Aβ burden in embryonic hippocampal neurons [140].

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