Neurolipofuscin in Aging and Aluminum-Induced Aging: Possible Therapeutic Interventions

摘要: Neurolipofuscin is considered a reliable biomarker of aging. Accumulating evidence indicates that it not simply an inert, harmless, wear and tear pigment but distorts the protein building machinery cell interferes with important autophagic process. Numerous forms cellular stresses activate macroautophagy. Increased vacuoles (AVs) are associated only aging ceroid disorders also Alzheimer’s disease. Mitochondria may have means for specifically targeting macroautophagy degradation which would be particularly healthy long axons distal terminals. The decomposition mitochondrial material source lipofuscin, at same time key to understanding mechanism Lipofuscin become indigestible because proteins ‘fixed’ via aldehyde bridges between amino groups. increasing proportion defective mitochondria ever decreasing supply functional lysosomes postulated hasten senescence and/or demise postmitotic cells. Oxidatively damaged contain some already peroxidized undegradable macromolecules. Brain aluminum content known increase age Aluminum toxicity might one underlying causes Alzhemier’s Accumulation this element in aged neurons has been demonstrated along increment lipofuscin. Both iron bind transferrin receptor before crossing blood-brain barrier mediated endocystosis. High level iron, concomitant increased content, detected rat brain. chronic administration accelerates A number antioxidants reported decrease lipofuscin neurons. Centrophenoxine facilitates elimination Also, citiolone retards lipofuscinogenesis. Recently, Ayurvedic herbal remedies, such as Maharishi Amrit Kalash, found reduce lipid peroxidation deposition. Administration extract Bacopa monnieri, possesses strong antioxidant activity, successfully reduced subjected aluminum-induced We thus conclude accumulation dysfunctioning reactive oxygen species significant indicator aging—perhaps even central our complex phenomenon