...ole in the explanation of aging, in general. In this moment, it is unclear if the mitocondria is the only energetical resource of the cell and is afirmed that a method for preventing or sloing loss of cognitive function may be as simple as maintaining adequate blood glucose levels. Skolnick, Andre A. JAMA, Chicago Apr 22, 1992 Gold2. THE SPEED AND THE HUMAN COGNITIVE AGINGIn accord ith the hypothesis of Bartzokis, the speed has an important role in the explanation of cognitive aging. More precisely, the author refers at the speed of transmission of electrical signals trough the neurons axons. The speed ould make it possible the integration of the information encoded distributively along and through the extended areas of some neuronal netorks. The integration of information distributed along the areas of some extended neuronal netorks is essential for the realization of the higher-order cognitive functions. Additionally, if not even alternatively, some scientists consider that, the stability that is represented by the state of brain beteen some biotemporal limits is in fact an equilibrium beteen some regenerative and degenerative processes. Regeneration can mean neurogenesis and synaptogenesis. Degeneration can mean apoptotic neuronal losses andor qualitative deterioration of the brains cells.That is, on the one hand it is sustained a reduction of the speed of transmission of the potentials of action, therefore a negative change of the quality of interneuronal communication, on the other hand it is sustained an unbalance beteen the proportion of regeneration and that of degeneration. Certainly, all this facts are effects of some physiological causes and ill have a biophysical and biochemical explanation, but maybe e ill have also a need of a specific philosophical or philosophico-scientific interpretation. It seems that, the continuous diminution of the neuronal quantity and quality, the diminution of the speed of transmission of the electrical signals that is caused by some neuronal qualitative changes of myelin sheath as el as the reduction of the interneuronal connections of the number and of the density of synapses have a fundamental role in the explanation of the neurocognitive aging.Bartzokis postulated and argued that, on the speed of trasmission depend many capacities of the neurocognitive system the quality of the interneuronal communication, the quality of integration of informations encoded distributedly on extended cortical spaces, and the temporal encoding of information. The induction of the same types of quantitative, qualitative, and relational changes in an artificial cognitive netork, ould have to mime the negative cognitive changes and trajectories associated ith aging and ith the degenerative disorders of the aging-related diseases.Bartzokis relationed a fundamental neurocognitive hypothesis about the importance of the syncrony in the higher cognitive functions ith the observations from the psychology of AD memory deficits and ith neurobiologic observations and hypotheses about the characteristics of AD extra and intraneuronal toxic deposits, neuronal losses etc.. Moreover, he provided detailed explanations of the concrete neurophysiological mechanims by hich have place the neuroquantitative, the neuroqualitative, and the neurorelational negative changes. The toxicity and the programmed death have an important role in the case of neuronal death. In conformity ith Bartzokiss model, the sheath of myelin have multiple functions the saltatory conduction by depolarization, hypopolarization, and hyperpolarization and the increase of the transmission speed of electrical signals, but also a protective role.Thus, the loss or the insuficiency of myelin affects both the speed and the protection. Due the fact that, the quality thickness of the myelin sheath in those regions of brain hich are myelinated late in life is inferior, that is hy those regions are lesioned ith selectivity. That is, the inferiority eakness of the myelinic protective quality of some cerebral regions ould explain their special vulnerability or preferential deterioration under the influence of oxidative stress and of the toxic deposits. A protective qualitative inferiority of some neuronal structures makes possible, conditionate not cause, their greater vulnerability.Certainly, the scientific and philosophical explanation of aging is in an non-definitive hystorical cognitive stage neither the neurocognitive explanation of memory can be reduced only to the relevation of importance of speed for syncronization nor the detailed explanation of the neurophysiological and neurochemical mechanisms hich determ the quantitative, qualitative, and relational negative changes of the brains cells is complete. Hoever, important advances ere realized. Additional to the decrease of speed, if it is true that, the memories are encoded in the interneuronal connections, than the neuronal losses, and therefore their syncronous synaptic losses, should have also a role in the age-related decrease of the mnezic function. Even if e dont understand completely and intelligiblely the function of the machinery of memory, e kno that all the cognitive functions are dependent fundamentaly on the neuroqantitative, neuroqalitative, neurorelational characteristics. That is hy, the struggle and the prevention of the cognitive aging impliesthe struggle of the neuroqantitative losses.the recovery of the neuroquantitative losses.the prevention of the neuroquantative losses.the struggle of deteriorative neuroqualitative changes.the improvement of the neuroqualitative characteristics.the prevention of the deteriorative neuroqualitative changes.the struggle of the interneuronal communicative relations losses.the multiplication of the interneuronal comunicative relations.the prevention of the relational losses.and, if some negative characteristics are essential to prevent the cancer, than the regulation of the negative and positive characteristics toards an optimum equilibrium.A part of the cognitive aging is rooted in the lesions caused by the oxidative stress and is conditioned by the neuronal protective eakness. Thus, the existence of the oxidative stress seems a condition of the possibility of the lesions due the interactions beteen the reactive oxigen species and the protective membranes. The elimination of the oxidative stress ould equivalate ith eradication of some phenotypes of aging, but this task maybe is too hard no, if not forever irealizable. That is hy, more realizable, no, ould seem, the decrease of the oxidative stress, or of its nocive effects, and the strenghtening of protection. The decrease of stress and the increase of protection. Also, the reduction and the prevention of the inter and extraneuronal toxicity ould have a therapeutical antisenectogen influence. The discovery of alternative means for the compensation of the transmission speed and for the neuronal protection ould seem usefull for the advancement of ...
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