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P3‐039: Aβ binding properties of a synthetic peptide corresponding to an amino acid sequence in human pericentriolar material 1 (PCM‐1) protein
Author(s) -
Chakravarthy Balu,
Atkinson Trevor,
Brown Leslie,
Menard Michel,
Ito Shingo,
Whitfield James
Publication year - 2012
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.05.1257
Subject(s) - microbiology and biotechnology , peptide sequence , peptide , biochemistry , amino acid , western blot , binding protein , polyclonal antibodies , biology , chemistry , antibody , immunology , gene
role and underlying mechanisms has not been fully understood. Hyperphosphorylated tau is the major component of Neurofibrillary Tangles (NFTs), which is one of the chracteristic hallmarks of AD. In the present study, the direct effect of Helicobacter pylori on tau phosphorylation, learning and memory are investigated. Methods: C57BLmice (3 months) were received Morris Water Maze training for 7 days and then divided into experimental group for intraperitoneal injection with conditional components of Helicobacter pylori (bacteria were incubated with culture medium for 30 min, then all the bacteria were removed to get the conditional medium), and control group for intraperitoneal injection with culture medium for 7 days. Then, the memory and learning abilities were detected by recording the latency (memory) and swimming strategy for the hidden platform with altered location. The mice were sacrificed and the hippocampus was homogenated, the phosphorylation levels of tau were detected by Western blotting. The same experiment was further repeated in N2a cells, cells were cultured in conditional medium for 24, 36, and 48 hours, the phosphorylation levels of tau were detected. Results: Conditional components of Helicobacter pylori treatment-induced cognitive impairment and tau hyperphosphorylation at several AD-tau hyperphosphorylation sites such as Ser214,Ser404, Thr205 and Thr231 both in mice brains and N2a cells, no change of total-tau level was observed. Conclusions: We conclude that conditional components of Helicobacter pylori impair the learning and memory ability, and directly induce tau hyperphosphorylation both in vivo and in vitro, peripheral infection with Helicobacter pylori may induce AD like pathogenesis through the release of toxins which could be sensed by the neurons.