THE PHILOSOPHICAL THINKING AND THE AGING Abstract. My metaintention is to promote a philosophy of the science of explanation and control of aging. Thus, in the fisrt part (1)., I consider the logicity of the scientific explanation of aging and I try to reduce the incompatibility between the philosophical rational model of explanation and the actual scientific explanations of aging. In the second part, I propose a categorical metaexplanation of the neurocognitive aging, analysing some results of neurobiology of aging and I propose a solution to a logical problem of explanation of aging. In the third part, I emphasize that, a complete explanation and understanding of aging requires also the knowledge of aging's conditions and I make the distinction between the conditions and causes of aging. In the fourth part, I propose a historical point for the emergence of aging and make an epistemological provocation. In the fifth part, I try to promote the fundamental principles of the eradication of aging. 1. THE LOGIC AND THE AGING 2. THE MIND AND THE AGING 3. THE CONDITIONALITY AND THE AGING 4. THE EVOLUTION AND THE AGING 5. THE PRIMITIVE PRINCIPLES OF THE ERADICATION OF AGING 1. THE LOGIC AND THE AGING How can be harmonized the scientific explanation of aging with the logic and the philosophy of science? The traditional Hempelian model (DN) of explanation was a deductive one. Hempel's model submsumes an individual event to a certain general law, an individuality to a generality. The generality can be unconditioned or conditioned. But, how can be modeled, in a similar way, the theories from the Medvedev's rational clasification? I consider that, most theories clasified by Medvedev are causaly explanatory. A set of phenotypes causes aging's phenotypes. For instance, ROS causes lesions, lesions also mean aging, aging is caused also by ROS. Or, myelin's deterioration or thiness causes the decrease of the protective power of the neuron. That decrease causes vulnerability to certain physical stressors. That is why, the neuronal death is conditioned also by the loss or deterioration of myelin. Important age-related neuronal losses causes cognitive aging. Telomeric changes causes replicative senescence (Hayflick, 1983). That is why, it seems that, we can formalize conjunctively Medvedev's clasification in the folowing way: (c1Ùc2Ù ...ÙcX) causes (e1Ùe2Ùe3Ù...ÙeX)=AGING. Where ci are causes and ei are effects. However, (c1, c2, ..., cX) can contain causes from different levels. Some causes do not determ directly behavioral aging, but there exist causal chains that determ only finaly behavioral aging. That is, there are indirect interactions between different levels (cognitive and non-cognitive, tissular and intracellular etc.), that is, certain bidirectionalities. Because all of this, the first premise of an explanatory reasoning cannot have, in our case, a simple 'C causes E' form. How simple was all in antiquity: P1: People are mortal. P2: Socrates is man. C: Socrates is mortal. or P1: People undergoes aging, naturaly. P2: Socrates is man. Condition1: are excluded the anti-aging actions. Condition2: is excluded the death by accident or incurable diseases. Conclusion: Socrates undergoes aging. P1: "ðx[(xIðH)®ðA(x)]. P2: Socrates belongs to H. C: Aging (Socrates). o r , "ðx[((xIðH)®ðA(x))Ùð(ðsIðH)]®ðAð(ðS). These reasonings extend a general intensional element to an individual that belong to a set-extension, but, it seems that, are non-explanatory. The characteristic or process that we have to explain is the characteristic of an object, a bio-object. Aging is not an absolute entity. However, we do not want to explain the aging of an individual man, but the human aging in general. The dificulty consists not in the extentension of a property to an individual, it seems. The actual scientific explanation of aging does not fit naturaly Hempel's model. We need a fundamental abstract understanding of aging. Aging implies quantitative and qualitative cellular changes. And also changes of the intercellular environment. Many aging-related quantitative cellular losses are caused by apoptosis conditioned by qualitative factors. The aging of the biowhole is not reducible to the loss of its fundamental redundat bioparts. Medvedev's rational clasification of the scientific theories of aging represents a multiplicity diversified in about six clases: 1. The theories of genetical programs. 2. The theories of the first lesions. 3. The theories based on the analysis of the manifestations of senescence at molecular, cellular, and organic levels. 4. The evolutionary theories. 5. The theories of aging of some particular tissues. 6. The unificatory theories. Considering this theoretical clases and trying to adapt them to the standard model of scientific explanation, I arrived at the folowing results: A. The causes and conditions of aging are present at different levels of the organisation of matter (f.i., atomic, molecular, tissular-cognitive); some conditions are even metaphysical: the absence of some perfect preventive and reparative mechanisms. That is why, a complete explanation cannot be causal and reductionist. B. There can be no a scientific complete biouniversal explanation of aging, in the sense that, the bioarchitectural differences bring new causes and conditions of aging which cannot be refounded in the explanation of other objects' aging. C. The standard model (DN) of scientific explanation implies the deduction or subsumation of an individual or particular case under a general case; the standard model's general is nomologic. This makes the first difficulty in the attempt of adaptation of the scientific explanation of aging, a complex reality, with the Hempelian nomological model of explanation. However, the problem of logical ordering of the explanation of aging become solvable, discovering the possibility of a regress to a more fundamental logicity. Thus, we can discover that between what explanates and what is explanated there have to be an implicative relation. What mens that, what explanates have to constitute a suficient condition to determ a necessary consequence-conclusion. Therefore, the theoretical corpus would have to form a suficient condition, for the derivation of an individual case, at least together with certain conditions. D. The discovery that, the disjunction or the conjunction of the theories of aging does not form a suficient condition for the derivation of conclusion about the aging of a concrete individual, until there is no an universaly accepted demonstration about the impossibility of eradication of aging. E. the discovery of some fundamental auxiliary conditions which can increase effectively the logical power of the explanatory reasoning: i) the exclusion of the anti-aging actions; thus, it is devisioused what is now the too hard problem of the possibility of eradication of aging. ii) the exclusion of accidental death. F. the understanding that, supposing the truth of all theories, their causes are suficient to effectuate aging, but if the list of causes is incomplete, than, on the one hand, the explanation substantiated by it will cannot predict with precision the mean trajectory of the process of aging, and, on the other hand, the strategical project designed to substantiate the actions for the eradication of aging founded on that list will be non-completely effective. 2. THE MIND AND THE AGING A superior part of the cognitive aging is caused by the loss of synchronization of the activities of some cognitive neuronal networks. This loss is caused by the decrease of the speed of transmission of action potentials. The decrease of speed is caused by a neuronal qualitative change, the alteration of myielin (Bartzokis, 2003), not by a by a cellular loss, which would mean a negative (quantitative) numerical cellular change. The speed of interneuronal communication depends on neuroqualitative characteristics. The neuron's main functional characteristics depend on the neuron's whole structure aleration and on the alteration of the interneuronal environment. Some alterations are clearly directly destructive, as those caused by ROS' action, some aging-related alterations, it seems that, are not de-structurative, as are the cross-links. The relations between the neuronal cells are comunicative and are important for the causation and conditionation of the higher order cognitive capacities. That is, they also are important in the explanation of the CNS' aging. Considering the senses of the main causes of aging presented actualy in the science of aging, I consider that aging implies: i) quantitative (numerical) cellular alterations. ii) qualitative cellular alterations. iii) and alterations of the intercellular environment (Campisi, 2003). Development also implies alterations, that is why I have to make further distinctions. Thus, the quantitative cellular alterations which are related to aging are negative numerical cellular alterations (cellular losses). Between the main special categorias of fundamental qualitative cellular alterations which mean or are first order aging effects are: the lesions (f.i., electron losses, molecular breakings), the sediment cumulations (f.i., beta amyloid, neuritic plaques), and the interconnections (molecular cross-links), and the spatial structure alterations (neurofibrilary tangles). An important philosophical intention, task, and problem is that of the adaptation of the scientific explanatory diverse with a fundamental rational model of scientific explanation. But, how can be adapted the explanation of the CNS's aging with Hempel's model of explanation. Or, how can be explanated the CNS's aging in a rational, logical, and abstract way? By the Hempelian model, an individual instance is subsumed under a general case, law, proposition, but the hard explanatory problem, it seems that, is not to subsume an individual under a general, but to derive the general from 'some' cases, from a particular. Scientists do not investigated all the brains from the world, to explain the brain's aging. Again, the dificulty is not to deduce an individual case from a general case, but to found the first premise, the general law, or the general case. After the general case will be founded, the derivation of an individual case from the general case will be an easy work. I think that, the investigation of all cases is a too uneconomic strategy for the scientific intelligence, cause this would require too much effort. The explanation of aging of an individual case will be suficient to extend the explanation on, or to cover with this explanation, the aging of all the brains that are suficient of similar with respect to their structural, quantitative, qualitative, and environmental characteristics. If we understood the capacities, functions, characteristics, of an individual object, than we can extend, at least in general, that understanding to all the objects that are suficient of similar with respect to their structural, quantitive, qualitative, environmental conditions and characteristics. That is, I think that, is unrational to consider that, objects that are very much similar with respect to their structural, quantitative, and qualitative characteristics can have very different capacities and functions, or there can be no different fundametal explanations of aging, for objects that are fundamentaly similar with respect to their compositional, structural, quantitative, and qualitative characteristics. There have to be a suficient reason, to give a explanation for fact. There have to be a suficient reason for an explanatory change rather than for an explanatory stability. There have to be a suficient reason for a change rather than for an non-change. The proportion of the change have to be directly proportional with the proportion of alteration, with the loss of identity. 3. THE EVOLUTION AND THE AGING The evolutionary theory of aging is a genetical theory of aging: the overall program of senescence is caused by effector and regulator genes, in accord with it. The firsts thinkers (see Clark:Reflections on an unsolved problem of biology: the evolution of senescence and death) that proposed this theory considered that, this genes were positively selected cumulatively and randomly by a process called antagonistic pleiotropy, cause they have a positive effect on, or favorize, reproduction. In the light of the recent advances of the molecular genetics, Clark criticized some of the earlier components or elements of the theory (f.i., the notion of antagonistic pleiotropy). Clark preserved the distinction between "senescence effector genes" and "senescence regulator genes". The main personal contribution of Clark, in his article Reflections on an unsolved problem of biology: the evolution of senescence and death, was about the evolutionary historical point (after or before the emergence of eukariotes) in which this genes emerged and about two radical new biological parameters by which that genes were selected: endosymbiosis with oxygen-metabolizing prokaryotes, and the use of sex in reproduction. The evolutionary theory of aging is the theory about the origin, accumulation, preservation, and the selective mechanisms of the genes that cause or regulate the senescence. A fundamental supossition of the evolutionary theory of aging is that, a gene can cause aging. But, the genes can be realy causes of aging? If A causes B, and B causes C, than A causes C? Or, if C causes D, and...N-1 causes N, than A causes N? That is why, there have to be first order aging-effects. For instance, the DNA microlesions are first order effects-aging? This microlesions can be caused by ROS, but the precursors of ROS can cause lesions, that is, are causes of aging? The non-reactive species of oxigen can cause lesions? The precursors of oxigen can cause aging-lesion-effects? We would can regress thus until to the strings, superstrings, and to the theory of everithing or until to the origin of the universe. The main categorias of the first order aging-effects are the lesions, the cross-links, the noxious sediments, the replicative impossibility etc. Cellular losses are undercaused be qualitative cellular changes. That is why, the main categorias of causes of aging are their imediat causes. That is, if and only if the gene cannot cause directly first order aging-effects, than there can be no genes that cause aging, but they are only some non-suficient conditions of a part of the complex reality of aging. I agreed that, the genetical level can conditionate aging, but I agreed neither with the hypothesis that genes subdeterm the overall program of senescence nor with the supossition that the fundamental conditions of aging are set of genes. The genetical level is vulnerable, deteriorable, lesionable, breakable, unstable (Eremia, 1997). The ___________expression of some genetical changes can cause non-functioning proteins. Maybe, some genetical expressions can give rise to noxious sediments or to precursors of the noxious sediments. It seems that, the toxicity is a fundamental independent cause of aging, but if it acts only by lesions, than is no more an independent cause. The non-suficient number of correct proteins can conditionate aging. All the genes and the DNA chains are vulnerable under the more fundamental pressure of time. I consider and I predict that, the first bio-object or the first living-structure was vulnerable, deteriorable, noxious sediments cumulativeable, that is agingable. That is, from the very beginig of the history of life, life was agingable or vulnerable to the fundamental pressure of time. In the actual light of the recent advances of the science of the explanation and of control of aging, it is unreasonable to imagine that there are or there were once cellular membranes that are or that were once unvulnerable, undeteriorable, unlesionable, unalterable with time. It seems that, there are no any cellular parts that are unvulnerable, undeteriorable, unalterable by the interaction with the fundamental physical stresors or by cross-links. A lesion is a breaking or ... a tearing out of a part from a whole or from a structure. For instance, an electron can be teared out from an atom, an atom can be teared out from a molecule, a molecule can be decomposed etc. A fundamental particle can undergo fision or desintegration. On the other hand, a cross-linkage is an intermolecular connection. ROS are more fundamental than the intemolecular connections, but the late are not solved as effects of the firsts. However, the accumulation of both are conditionated by some atractive force fields and by the absence of some perfect preventive and reparative mechanisms. The replicative impossibility is not the ___________expression of a gene, but is caused by the loss of the telomeres' caps, but is conditioned by an imperfect replicative mechanism that substantiates only a finite replicative capacity. In the light of the recent advances of the science of explanation and manipulation of aging, I propose that, there were never bio-objects that were unvulnerable by the interaction with the fundamental physical lesators. I propose the folowing epistemological chalenge, all the so called imortal cells are agingable, that is are vulnerable, deteriorable, lesable with time, at least in very big periods of time. 4.THE CONDITIONALITY AND THE AGING The maintenance of the cellular structures requires the assimilation of new proteins, cause the cellular structures are vulnerable to protein losses. The genetical level, which contain protein patterns, is also vulnerable to physical lesators. The ___________expression of a lesated protein pattern can give rise to non-functioning or non-useable proteins. The absence of correct proteins can conditionate a part of aging. But can this absence to be causal? No. The nothing or the non-being cannot act causaly on the matter. Than what is the clear explanation of this part of aging? The protein has also the role of being as a matter of construction. The non-maintenance of the cellular structures is, commonly, caused also by protein losses. Ussualy the absence of new correct suplimentary proteins is a suficient condition, if the the protein losses are inevitable, for the succesion of a first order aging-efect. That is, a part of aging means a structural alteration caused by losses that are suficiently conditioned by the absence of some supplements. The absence of some perfect preventive and reparative mechanisms is a suficient condition to permit the actions that promote the aging. What will seem interestingly, for the philosophers of science, maybe, will be that a suficient condition can be non-causal and non-matterial. 5. THE PRIMITIVE PRINCIPLES OF THE ERADICATION OF AGING The science of aging is oriented both towards the explanation and eradication of aging. The eradication of the behavioral aging can be substantiated, at least partly, cause aging can be promoted also from the behavioral level, by the eradication of the first order aging-effects. The eradication of an effect can be substantiated by the manipulation of its cause or causes. However, this principle is an aging-preventive one, but we need an aging manipulative principle. It seems that, some fundamental categorias of first order aging-effects are the lessions and the cross-links. That is, some breakings and some connections. That is why, some fundamental principles for the antiaging manipulation would can be the reconnection of the breakings and the separation of the cross-links. However, at this stage of the scientific knowledge and technology, it seems to me that, the application of the previous principle would be too hard. That is why, we need a simpler case, for the begining. We have to humiliate us, maybe, and to choose a simple concrete aging-efect or aging-cause. Thus, from the category of noxious sediments we would can choose the beta-amyloid noxious compounds. The body cannot decompose this noxious compounds, by itself. To struggle this noxious compound we would have to solve two subproblems: P1) the problem of recognition only of beta-amyloid compounds. P2) the problem of the decomposition only of the beta-amyloid compounds. Thus, we would need a way to act in this senses either from the outside or the inside of the organism. References: Bartzokis, G.:2003, Age-related myelin breakdown: a developmental model of cognitive aging and Alzheimer's desease, Neurobiology of aging. Campisi, Y.: 2003, Cellular senescence and apoptosis: how cellular responses might influence aging phenotypes, Experimental Gerontology. Clark, W.R.:Reflections on an unsolved problem of biology: the evolution of senescence and death , in W R Clarkwebsite. Eremia, D.: 1997, Structurile vii sub presiunea timpului, Editura All, Bucureºti. Hayflick, L.: 1983, Theories of aging, in Fundamentals of Geriatrics medicine eds. R.D.T. Cape, R.M. and J. Rossman Raven Press, New York, 43-50. Hempel, C.G.,:1965, Aspects of Scientific Explanation, in Aspects of Scientific Explanation and other Essays in the philosophy of science, The Free Press, New York. Medvedev, Z.A.: 1990, An attempt at a rational clasification of theories of aging, Biol. Rev., 65, 375-398.
