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P1‐148: Mechanisms of dietary docosahexaenoic acid‐induced protection against and amelioration of impairment of memory learning ability in Alzheimer's disease model rats
Author(s) -
Hossain Md. S.,
Hashimoto Michio,
Yamashita Shinji,
Katakura Masanori,
Tanabe Yoko,
Fujiwara Hironori,
Gamoh Shuji,
Miyazawa Teruo,
Arai Noriyuki,
Shimada Toshio,
Shido Osamu
Publication year - 2008
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.2008.05.735
Subject(s) - docosahexaenoic acid , thioflavin , chemistry , cholesterol , polyunsaturated fatty acid , in vivo , medicine , biochemistry , endocrinology , amyloid (mycology) , alzheimer's disease , fatty acid , biology , disease , microbiology and biotechnology , inorganic chemistry
Male Wistar rats aged 24 month old divided into two groups of 10 rats each: A). control treated with 0.2ul saline solution intra HT for two weeks, Group B treated with o.5M Glu 0.2 ul intra HT. Incubation of brain fragments with 45CaCl2 10ul/sample has been done using a Beta Berthold Scintilator Counter. Results: Bioelectric activity of HT and neocortex was similar of that of narcotic sleep delta-teta waves were predominant with frequences raning between 0.3-0.5 cici/second 40-80 microvolts amplitude. 10 minutes after injection there is an accelerated depletion of intracellular ATP which is the main event installed before the onset of other phenomena, the accelerated tendency of discharge of frequency is more evident at cortical level followed by a depression of waves frequency suggesting thus an initial excitation followed by an inhibition state of bioelectric activity.The acceleration of discharge frequency phenomena of waves were followed by depression of waves amplitude in HT esspecialy in neocortex suggesting an initial excitation produced by Glu administration as in Parkinsonian simptoms respectively.Intra HT injection of Glu determines an increased reactivity of HT and neocortex also, triggering neurotoxical effects esspecialy at the HT level, the effects have been similar to those reported in the case of neurodegenerative disorders in humans. Conclusions: Excessive influx of Ca into depolarised neurons has been proposed as the mechanism by which excitotoxins induce neuron cell death. The excitotoxic stimulation of neurons induce hypoxia/ischemia conditions similary as in neurodegenerative disorders of aging people with very important implications for understanding the exitotoxic mechanism. Glu could be a main factor in the onset of neuronal cell death by changing the cell energetics, and of redox cellular potential due to the decrease capacity of free radicals inactivation.