Alzheimer’s disease represents one of the main health problems in advanced countries. Actually, we do not have an effective therapy for disease and its cause remains unknown. For several decades, research has focused on amyloidogenesis as the primary cause of disease. However, clearly satisfactory results have not been obtained in this line of research. In recent years there has been growing evidence about the role of neuroinflammation in AD and other neurodegenerative diseases. The role of ß-Amyloid as an element of the innate immune response places it in a new position in the pathophysiology of the disease. Alterations of intestinal and oral microbiota could have a role in the generation of neuroinflammatory changes, either directly by pathogens or by bacterial endotoxins. Endotoxins are polysaccharides of gram-negative bacteria that produce a potent immune reaction. Recently, there is evidence that gingipains have a role in production of neurotoxicity and amyloidogenesis. Gingipains are endotoxins produced by a pathogen associated with chronic periodontitis, Porphyromonas gingivalis. Gingipains generate direct neurotoxicity and its effect could be reversed with various molecules that are currently under development.
neuroinflammation
Bacterias, Endotoxinas y Neuroinflamación Crónica: ¿Una Etiopatogenia Para las Enfermedad de Alzheimer? Bacteria, Endotoxins And Chronic Neuroinflammation: An Etiopathogenesis For Alzheimer’s Disease?
Esclerosis Múltiple y neuroplasticidad: Eventos en la patogenia y proyecciones terapéuticas.
Several forms of neural plasticity can occur in the adult Nervous System activated by experience and regulated by the interaction among the environment, stress, physical exercises, and physiological conditions (i.e. pregnancy). Recent studies demonstrate that specific neuroplastic events occur in Multiple Sclerosis (MS) and its experimental animal model, as well as some punctuate failures in neuroplastic mechanisms. Basic pathogenic mechanisms of MS related to axonal and myelin integrity loss and associated to inflammation processes and the dual roll of inflammation in the neurodegeneration/neuroprotection relation are reviewed. We emphasize in the actual therapies trends in those topics and in the current evidences of neuroplastic changes in MS.
