ACAID as a potential therapeutic approach to modulate inflammation in neurodegenerative diseases. (March 2016)

• Record Type: Journal Article
• Authors: Toscano-Tejeida, D.; Ibarra, A.; Phillips-Farfán, B.V.; Fuentes-Farías, A.L.; Meléndez-Herrera, E.
• Is Part Of: Medical hypotheses. Volume 88(2016)
• Page Start: 38
• Page End: 45
• Publication Date: 2016-03
• Subjects: Medicine -- Periodicals; Medicine -- Periodicals; Médecine -- Périodiques; Medicine; Periodicals; 610
• DOI: 10.1016/j.mehy.2016.01.006
• Languages: English
• ISSNs: 0306-9877

Abstract

Abstract: The progressive loss of neurons and inflammation characterizes neurodegenerative diseases. Although the etiology, progression and outcome of different neurodegenerative diseases are varied, they share chronic inflammation maintained largely by central nervous system (CNS)-derived antigens recognized by T cells. Inflammation can be beneficial by recruiting immune cells to kill pathogens or to clear cell debris resulting from the primary insult. However, chronic inflammation exacerbates and perpetuates tissue damage. An increasing number of therapies that attempt to modulate neuroinflammation have been developed. However, so far none has succeeded in decreasing the secondary damage associated with chronic inflammation. A potential strategy to modulate the immune system is related to the induction of tolerance to CNS antigens. In this line, it is our hypothesis that this could be accomplished by using anterior chamber associated immune deviation (ACAID) as a strategy. Thus, we review current knowledge regarding some neurodegenerative diseases and the associated immune response that causes inflammation. In addition, we discuss further our hypothesis of the possible usefulness of ACAID as a therapeutic strategy to ameliorate damage to the CNS.