Amyloid β peptide, which is aggregated extracellularly in the neuritic plaques, generates a constant inflammatory environment and prolonged, activation of microglial and astroglial cells that potentiate neuronal damage and have been involved in the alteration of the BBB, damaging the permeability of blood vessels. Maybe as a consequence of degradation of tight junctions proteins, favouring the loss of these junctions, altering the permeability of blood vessels. Understanding the mechanisms of action of different species of beta amyloid peptide could lead to new therapeutic interventions directed to inhibit Aβ aggregation at the level of oligomers, which are much more toxic than the fibrillary form. It is important to understand the mechanisms of action of caspase-5, in this pathological process of amyloid β peptide, emphasizing the clinical importance of casapasa-5 and its relation to the process of neuroin‐ flammation.
Soto-Rojas, L. O., Cruz-López, F. de la, Ontiveros-Torres, M. A., Viramontes-Pintos, A., Cárdenas-Aguayo, M. del C., Meraz-Ríos, M. A., … Luna-Muñoz, J. (2015). Neuroinflammation and Alteration of the Blood-Brain Barrier in Alzheimer´s Disease. In Alzheimer’s Disease - Challenges for the Future. InTech. https://doi.org/10.5772/60024