Aβ aggregation and Tau phosphorylation suggest PhIP correlation to Alzheimer’s disease Bhavya Patel
PhIP, 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine, is a dietary heterocyclic aromatic amine that is chemically released when cooking meat at increased temperatures. Syeda et al. (2020) examines the correlation between PhIP exposure and the neuropathology of AD. The authors experimented on C57BL/6 mice and divided them into three groups that experienced differing levels of PhIP exposure. A 6-7 week old male and female group of mice were treated with 100/200 mg PhIP/kg for 8 hours once a week. The next group consisted of 8-9 week old male mice exposed to 75mg PhIP/kg for a period of 4 weeks(3x/week) and the last group was injected with 75mg PhIP/ kg for 16 weeks(3x/week). The control for each group was a vehicle treated group injected only with corn oil. Mice were then decapitated, brains were divided into two halves and stored in liquid nitrogen for further processing. Assessments included measuring oxidative damage through ChAT positive cells in the striatal region, synaptic alterations in the hippocampus, and inflammation via GFAP intensity. BACE1, APP, Aβ and tau protein phosphorylation was compared between each group of mice and control. An accumulation of Aβ and tau-phosphorylation are major characteristics of AD and are prominently seen in the 16-week group. Furthermore, oxidative stress is increased in the hippocampus suggesting that the mechanism of Aβ aggregation via PhIP may be a result of BACE1 and APP upregulation. A summary of results is indicated in Figure 1.
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