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Cerebral Erythropoietin and Neurodegenerative Diseases

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Never before has humanity compiled so much information about Human anatomy and particularly the brain. Paradoxically, this knowledge has not yet been transformed into a favorable impact against neurodegenerative diseases. Moreover, these pathologies, which include Alzheimer's disease, Parkinson's disease and ...

Never before has humanity compiled so much information about Human anatomy and particularly the brain. Paradoxically, this knowledge has not yet been transformed into a favorable impact against neurodegenerative diseases. Moreover, these pathologies, which include Alzheimer's disease, Parkinson's disease and mental disorders such as major depression, show increased incidences, as a logical consequence of the augmentation of life expectancy for the society as a whole, and age constitutes their main risk factor. Without a doubt, it is a necessity for the neuroscientific community to offer new paradigms that allow to define innovative prophylactic and therapeutic approaches against neurodegenerative diseases. In Alzheimer's disease for instance, many theories have arisen during the past century that have led researchers to develop drugs targeting accumulation and/or formation of Tau or beta-amyloid proteins. After marginal successes in complex experimental models, all trials failed in clinical studies. The fundamental causes of these failures are the toxicity or lack of efficacy of the studied drug in Humans.

In facing such a bleak outlook, it seems logical to question the hypotheses we have handled and to remember that there is nothing more practical than a good theory. In this direction, and with the briefly presented background, we propose to consider that what happens in these diseases, both clinical and neurochemical symptoms are no more than the consequences of a primary phenomenon that alters the complex skein or framework of brain homeostasis leading to physiological alterations. This triggering factor can be a xenobiotic of exogenous or endogenous origin that under normal conditions can be eliminated but, when faults, becomes slowly lethal for neuronal systems. In this regard, metabolic crossroads is a critical point where the processes related to cell life or death are defined. Erythropoietin (EPO) is a likely candidate to confirm this hypothesis. Indeed, erythropoietin is produced in the brain and appears to be one of the fundamental metabolic crossroads between neurons, glial cells and vascular cells, which can tip the balance to processes of repair or death of neuronal and non-neuronal populations. Actually, it is striking to understand why the brain, an organ with highly selective physiological needs, develops, as soon as very early stages of development, its own production of the cytokine, which, apparently, is maintained throughout life. An alteration of the endogenous cerebral EPO (CEPO) homeostasis could be the cause of alterations of the neurovascular unit and specific circuits, leading to inadequate trophic and tropic supports, including BDNF system, and neuronal loss. This putative alterations will affect specific regions according to the damage caused and therefore it could have causal importance in different neurodegenerative diseases.

All interested neuroscientists are welcome to open the debate, bringing their support, judgment and original ideas to explore this new hypotheses. We initiate this action with the deep conviction that a multidisciplinary and multicultural forum of exchange will benefit to the field and more broadly to the emergence of innovative concepts in neuroscience.


Keywords: Human, Brain, EPO, Erythropoietin, Neurodegenerative Diseases


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