a search for mitochondrial damage in alzheimer’s disease using isolated rat brain mitochondria

Authors

jalal pourahmad -

mehrdad faizi department of pharmacology and toxicology, faculty of pharmacy, shahid beheshti university of medical sciences, p.o. box 14155-6153, tehran, iran.

enayatollah seydi department of pharmacology and toxicology, faculty of pharmacy, shahid beheshti university of medical sciences, p.o. box 14155-6153, tehran, iran.

sadegh abarghuyi faculty of pharmacy, shahid beheshti university of medical sciences, p.o. box 14155-6153, tehran, iran.

abstract

alzheimer’s disease (ad) is a progressive neurodegenerative disorder that affects regions of the brain that control cognition, memory, language, speech and awareness to one’s physical surroundings. the pathological initiation and progression of ad is highly complex and its prevalence is on the rise. in his study, alzheimer&apos;s disease was induced with single injection of amyloid-β (aβ) peptides (30ng, by stereotaxy) in each hemisphere of the brain. then memory dysfunction, oxidative stress and apoptosis induced by aβ peptide were investigated on isolated brain mitochondria obtained from infected rat. our results showed memory impairment in rats after receiving an aβ peptide. we also found significant rise (p<0.05) at ros formation, mitochondrial membrane depolarization, mitochondria swelling, cytochrome c release on mitochondria isolated from brain of these memory impaired rats compared with those of untreated control rat group. our results suggest that oxidative stress and mitochondria mediated apoptosis in brain neurons play very important role in initiation of ad.

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Journal title:
iranian journal of pharmaceutical research

جلد ۱۵، شماره Special Issue، صفحات ۱۸۵-۱۹۵

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