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An integral approach to the etiopathogenesis of human neurodegenerative diseases (HNDDs) and cancer. Possible therapeutic consequences within the frame of the trophic factor withdrawal syndrome (TFWS)
Authors:Salvador Harguindey  Gorka Orive  Ramn Cacabelos  Enrique Melndez Hevia  Ramn Díaz de Otazu  Jose Luis Arranz  and Eduardo Anitua
Institution:Salvador Harguindey, Gorka Orive, Ramón Cacabelos, Enrique Meléndez Hevia, Ramón Díaz de Otazu, Jose Luis Arranz, and Eduardo Anitua
Abstract:A novel and integral approach to the understanding of human neurodegenerative diseases (HNDDs) and cancer based upon the disruption of the intracellular dynamics of the hydrogen ion (H+) and its physiopathology, is advanced. From an etiopathological perspective, the activity and/or deficiency of different growth factors (GFs) in these pathologies are studied, and their relationships to intracellular acid-base homeostasis reviewed. Growth and trophic factor withdrawal in HNDDs indicate the need to further investigate the potential utilization of certain GFs in the treatment of Alzheimer disease and other neurodegenerative diseases. Platelet abnormalities and the therapeutic potential of platelet-derived growth factors in these pathologies, either through platelet transfusions or other clinical methods, are considered. Finally, the etiopathogenic mechanisms of apoptosis and antiapoptosis in HNDDs and cancer are viewed as opposite biochemical and biological disorders of cellular acid-base balance and their secondary effects on intracellular signaling pathways and aberrant cell metabolism are considered in the light of the both the seminal and most recent data available. The “trophic factor withdrawal syndrome” is described for the first time in English-speaking medical literature, as well as a Darwinian-like interpretation of cellular behavior related to specific and nonspecific aspects of cell biology.
Keywords:neurodegenerative diseases and growth factors  Alzheimer’s Disease  human neurodegenerative diseases  cancer  intracellular acid-base homeostasis  apoptosis  antiapoptosis  etiopathogenesis and treatment
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