An antistress and antiaging neurometabolic therapy. Accelerated lipofuscinolysis and stimulated anabolic regeneration by the antagonic-stress synergistic formula.
In both stress and aging, an etiopathogenic analysis demonstrates in the brain some common mechanisms and reciprocal accelerating relationships: hypoanabolism (decrease of RNA and protein synthesis), coupled with hypercatabolism (increase of oxidative stress-lipid peroxidation, with waste product accumulation: lipofuscinage pigment and water-insoluble proteins). For therapeutical intervention in these antihomeostatic processes, we successively (1972-1992) developed a neurometabolic antioxidative therapy--finally represented by a specific antistress and antiaging synergistic formula, Antagonic-Stress. Its homeostatic actions have been demonstrated in the stressed aging brains by reestablishing the anabolism/catabolism balance: anabolic regeneration by increasing total RNA, total proteins and water-soluble proteins, coupled with catabolic regulation by accelerated lipofuscinolysis and age pigment elimination (neuronal-->glial-->capillary route) and decreasing of water-insoluble proteins. Specific, synergistic, and superior actions of Antagonic-Stress multiple formula vs. antistress and antiaging monotherapy have been demonstrated by preclinical and clinical studies, confirming our results.
Riga
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Institute of Neurology and Psychiatry, Bucharest, Romania.
Riga
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D000375:Aging; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D001921:Brain / Q000378:metabolism*; D004247:DNA / Q000378:metabolism; D004734:Energy Metabolism; D008062:Lipofuscin / Q000378:metabolism*; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D012313:RNA / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000188:drug therapy / Q000378:metabolism*
D000975:Antioxidants; D008062:Lipofuscin; D009419:Nerve Tissue Proteins; D012313:RNA; D004247:DNA