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Fig. 1 | Alzheimer's Research & Therapy

Fig. 1

From: The pleiotropic role of p53 in functional/dysfunctional neurons: focus on pathogenesis and diagnosis of Alzheimer’s disease

Fig. 1

Exacerbation of AD pathology through gradual dysregulation of p53-induced adaptive responses. Upon chronic exposure to mild/subacute stress, p53 becomes activated through ROS or through the induction of DNA damage sensing genes, such as ATM kinase. Following p53 activation, several antioxidant genes (e.g., TIGAR, MnSOD, and PGC-1α) are upregulated to subsequently restore cellular damage. In the AD brain, levels of ATM are strongly upregulated. However, there appears to be a defect in the downstream canonical p53 pathway, as p53-induced adaptive responses are progressively dysregulated during the continuum of the disease, exacerbating AD pathology. AD, Alzheimer’s disease; ATM, ataxia-telangiectasia mutated; MnSOD, manganese superoxide dismutase; PGC-1α, peroxisome proliferator-activated receptor-c coactivator-1a; TIGAR, TP53-induced glycolysis regulatory phosphatase; ROS, reactive oxygen species

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