http://onlinelibrary.wiley.com/doi/10.1034/j.1600-079X.2003.00041.x/pdf
malatonin boosts antioxidant molecules!!
mTOR and Brain.
Since many neurodegenerative diseases are associated with accumulation of misfolded or aggregate prone proteins, rapamycin may be particularly relevant to neuronal health. Rapamycin both slows translation of new proteins and induces autophagy. Slowing down the rate of protein synthesis may make the cell more effective and clearing and removing misfolded or damaged proteins. Additionally, slowing protein synthesis may be a cue for neurons to upregulate machinery to cope with damaged proteins, oxidative damage, and other stressors. Beyond slowing the production of proteins, the induction of autophagy by rapamycin can clear damaged organelles or proteins that are resistant to degradation by the proteosome. Furthermore, brain specific removal of ATG5 or ATG7 (Hara et al., 2006 T. Hara, K. Nakamura, M. Matsui, A. Yamamoto, Y. Nakahara, R. Suzuki-Migishima, M. Yokoyama, K. Mishima, I. Saito, H. Okano and N. Mizushima, Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice, Nature 441 (2006), pp. 885–889. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (597)[Hara et al., 2006] and [Komatsu et al., 2006]), requirements of autophagy, are sufficient to induce neurodegeneration in mice, suggesting that autophagy is required for normal maintenance in neurons. Thus, the duel actions of rapamycin on protein turnover may support neuronal well-being by slowing production and increasing removal of damaged material.
In healthy neurons, the mTORC1 signaling pathway can respond to a variety of stimuli and trigger appropriate, long-lasting responses. The mTORC1 pathway is involved in synaptic plasticity, in part by coordinating the timing and location for the synthesis of new proteins. mTOR activity is used by the brain to monitor nutrient status, regulate feeding and consolidate long-term memories. However important the role of mTORC1 activity in the healthy brain, evidence is mounting that the diseased brain may benefit from reducing mTOR activity. Treatment with rapamycin benefits a range of models for Alzheimer's disease, Parkinson's disease, and polyglutamine expansion diseases. Further characterizing mechanisms by which rapamycin and its analogs reduce toxicity should yield promising potential therapies for these diseases: treatments that may alleviate pathology while sparing mTOR's ability to support normal brain function.
http://www.ncbi.nlm.nih.gov/pubmed/20849946
ci sono dati che dicono che la lifespan massima può essere considerevolmente aumentata inducendo l'autofagia nel solo sistema nervoso centrale. Ora, credo che per una sorta di bilancio proteico se si induce il trofismo muscolare si riduce la disponibilità di amminoacidi liberi per il cervello, inducendo così la risposta autofagica per riciclare proteine già sintetizzate e liberare amminoacidi sufficianti per la trascrizione proteica. Leggevo del resto che l'attivtà fisica diminuisce i livelli di glutammato (neurotossico oltre una certa soglia) nel cervello per via del fatto che il glutammato viene impiegato come substrato energetico.
Quindi può essere che un po' di sana palestra sia una pratica protettiva e anti-aging-
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