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Life implies time. The biotime of a human being has two main components: the development-time and the aging-time. Life is temporal. Thus, there is a succesion of changes from birth until to death, in the case of human being. Here, I want to appreciate, again, some of the main causes and conditions on which aging depends.


Aging is a process, but is a process that affects either an unicellular or a multicellular object. That is why, aging have to be a process that affects the cells. The cells are micro-objects of which functional characteristics depend on their compositional and structural characteristics. Being open and active systems, the cells consume energy. Every activity implies energy consumption. The reduction of energetical resources affects the activity or the functioning of cells. That is, it is supossed that, the continuous reduction of the energetical resources of cells causes a continuos reduction of the activity or functioning of cells. (Skolnick, Andrew A. JAMA . Chicago: Apr 22, 1992). The later reduction means and causaly explain a part of aging. The subcause of this reduction-cause are the accumulation of the genetical or lesional alterations of mitocondrias, which are the main energetical resources of cells, which make them non-functional. That is, the reduction of the cellular energetical resources has a causal role 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 slowing loss of cognitive function may be as simple as maintaining adequate blood glucose levels". (Skolnick, Andrew A. JAMA, Chicago: Apr 22, 1992; Gold)


In accord with 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 would make it possible the integration of the information encoded distributively along and through the extended areas of some neuronal networks. The integration of information distributed along the areas of some extended neuronal networks 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 between some biotemporal limits is in fact an equilibrium between some regenerative and degenerative processes. Regeneration can mean neurogenesis and synaptogenesis. Degeneration can mean apoptotic neuronal losses and/or qualitative deterioration of the brain’s 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 between the proportion of regeneration and that of degeneration. Certainly, all this facts are effects of some physiological causes and will have a biophysical and biochemical explanation, but maybe we will 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 wel 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 network, would have to mime the negative cognitive changes and trajectories associated with aging and with 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) with the observations from the psychology of AD (memory deficits) and with 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 which 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 with Bartzokis’s 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 which are myelinated late in life is inferior, that is why those regions are lesioned with selectivity. That is, the inferiority (weakness) of the myelinic protective quality of some cerebral regions would 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 which determ the quantitative, qualitative, and relational negative changes of the brain’s cells is complete. However, important advances were 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 we don’t understand completely and intelligiblely the function of the machinery of memory, we know that all the cognitive functions are dependent fundamentaly on the neuroqantitative, neuroqalitative, neurorelational characteristics. That is why, the struggle and the prevention of the cognitive aging implies:

the 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 towards 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 weakness. Thus, the existence of the oxidative stress seems a condition of the possibility of the lesions due the interactions between the reactive oxigen species and the protective membranes. The elimination of the oxidative stress would equivalate with eradication of some phenotypes of aging, but this task maybe is too hard now, if not forever irealizable. That is why, more realizable, now, would 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 would have a therapeutical antisenectogen influence. The discovery of alternative means for the compensation of the transmission speed and for the neuronal protection would seem usefull for the advancement of the science of the eradication of aging.


Can be reduced the explanation of the whole's aging at cellular losses? It is certain that, the neurquantitative changes (losses), the neuroqualitative changes (plaques or tangles, lesions, cross-links etc.), and the interneuronal environmental changes (toxical increases) can cause and/or conditionate cognitive aging and other neuronal disorders (AD). However, it seems that, this do not represent all the main kinds of first-order aging-effects. We have, in the abstract or categorical explanation of the human cognitive aging, the folowing kinds: neuronal losses and neuronal alterations. And the interneuronal environmental influences, maybe.

The complexity of brain-system-whole made me to anticipate that its structural properties will have a role in the explanation of the higher-order cognition's aging. The part-unity of the NS-whole is the neuron. The systematicity of the NS implies that there are interneuronal relations. That is, the specialization of the different neuronal areas and networks is made possible by the relations between neurons. The interneuronal relations have a communicative nature. The neurons encodes the information by the density and the temporal distribution of electrical impulses that they send to each other by the release and the reception of neurotransmiters. Additionaly to speed, there are researchers that consider that the density of the interneuronal synapses have an important role in the explanation of the human cognitive aging.

Moreover, "Terry, MD, professor of neurosciences and of pathology at the University of California, San Diego, speaking at the NIH conference, he said he and his colleagues found 'no significant decline in the total number of neurons in either midfrontal, superior, temporal, or inferior parietal areas.'"(Skolnick, Andrew A. JAMA, Chicago: Apr 22, 1992) But, instead, the normal elderly has about with 20% less mean sinapse density than a normal young and a person which sufers of the AD has about with 45% less synapses than a normal elderly. (Terry in Skolnick, Andrew A. JAMA, Chicago: Apr 22, 1992).


Certainly, aging is a complex reality, caused and conditionated by multiple factors. Medvedev's rational clasification of the theories of aging contains hundreds of theories. The causes of aging are certainly multiple, than the theoretical corpus which explains aging have to be complex. Than what is the true value of inference to the best explanation (IBE)? Have IBE an universal importance for the scientific explanation in general? No, in the interpretation that we should select only one theory.

But more important is that, aging in itself is not a phenomenon. By our senses and artificial instruments we can have phenomenons about aging, but aging itself is not a phenomenon. Our phenomena are caused and conditioned both by the stimuli between aging and our senses and by the functional architecture of our cognitive system. Instead of all this influences, our percepts preserve in some limits or grades some characteristics of the reality in itself. For instance, our neuronal networks which are correlated with the conscious vision are retinotopicaly organized. And our retinas are topographicaly organized. A part from our percepts is constituted by the stimuli itself, cause at the level of eyes the photons are converted in electric impulses. (Hubbel, Eye, Brain, and vision)

What seems true and acceptable is that, our cognitive contents that have the role to explain have to form a suficient reason for derivation of the cognitive contents that we want to explain, no matter how long and tangled would be the whole reasoning. There can be non-communicated explanations. Though that all our cognitive activities are substantiated by patterns of neuronal activitities, in the philosophy of scientific explanation we should be interested by their meaning or sense, validity, and efficiency, primarly. We would can corelate and interpretate neuronaly every explanation, even non-valid explanations. If we want to evaluate their importance and validity, we have to focus our atention on their meaning. At the level of meaning, that is the proper level, we have to analyse and evaluate the scientific explanations. It is absurd to say about a neuron's firing that is imoral, ilogic etc.

We should reject an exagerated revolutionary history in the explanation of aging, I propose. That is, a history that pass from a theory to other rejecting all the previous findings. We should integrate and coherentize all that is true. The progress implies a temporal accumulation of truths and/or a temporal rejection of falses. That is, the increase of true explanations and the decrease of false explanations. Our aim should be, I propose, the maximization of the best progress. The concrete scientific findings and explanations should be refined and coordinated from the highest conceptual level. The hardest work is made by experimental researchers.


Now, I want to appreciate the main kinds of first-order aging-effects. At intracellular level they are qualitative changes: lesions, cross-links, and the replicative senescence at the amitotic cells. That is, they mean certain disconnections, certain interconnections, and a certain (replicative) impossibility. The last is caused by a continuous erosion, disconnection. This effects are caused by the chemical interaction of the cellular parts with some atoms or molecules that are formed in the metabolical or fuctional processes of the cell. That is, different microfields of force mediate all this interactions, with negative or positive consecquences for the cellular substructures. The different fields of forces are responsible for all the atomic and molecular connections and disconnections. The fields of forces mediate all attractions and rejections.

At the tissular level we aging can mean: negative structural and quantitative changes. Thus, the negative quantitative change is the cellular losses. And, in the case of the neural tissue, the negative structural change is the loss of synapses, that is the loss of some communicative neuronal relations. An important cause of the cellular losses is apoptosis. The apoptosis is cased by qualitative alterations. That is, the quantitative changes are caused by qualitative changes.

At the level of the wole organism, a part of aging depends on the negative alteration of the relations between organs. The negative relational alteration depends on the aging-related negative alterations of the organs. The NS's aging cause a weaker control of the muscular system. The breathing system's aging cause, if the environmental conditions are identical, the decrease of the quantity of

disponible oxigen. The negative quantitative, qualitative, and structural alterations of NS cause the negative higher-order cognitive alterations. The negative higher-order cognitive alterations cause, if the environment remain the same, a decrease at behavioral level, a decrease of the capacity of surviving, a decrease in the capacity of solving the problems which struggle our happiness.


There are general intracellular conditions, cognitive conditions, and volitive conditions of aging. All this are inherent cognitions of aging, but, however, there are also social conditions and influences toward or against aging (f.i., gerontological societies). The main intracellular conditions of aging are the absence or the imperfection of the reparative, regenerative, replicative, and aging preventive mechanisms. There are many substances (vitamines (C, E, P), aminoacids (glutation, cistein) enzymes (-SH, Q10), pigments (carotenoids) etc.) that have a reparative, regenerative, and preventive action, but their efficiency is not perfect. This imperfection can conditionate, under other condition, accumulation with time of the first-order aging-effects.

But it seems that, the most important condition of aging, if the eradication of aging is not impossible by the nature of things in theirself, is a cognitive one: the ignorance. However, our ignorance is controled by our volition. But, though that our volition, it seems that, is simply positive, however, our volition would can be very coordinative and insistent...That is why, our ignorance depends on our evaluations and volitions... Our ignorance depends primarly on the validity of our reasonings, evaluations, and on the force and resistance of our volitions... The power of the gerontological group is conditioned by the intelligence of the cooperation between its members and on the intelligence of their coordination, both in short and long time. The historical progress of gerontological society is positively conditioned and caused by the the critical evaluation, interpretation, coherent harmonization, refinement, and integration of the true theoretical and experimental results of its past. l4f9fh

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