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Article type: Review Article
Authors: Arosio, Beatricea; b; * | Casati, Martinaa; c | Gussago, Cristinaa | Ferri, Evelyna; c | Abbate, Carlob | Scortichini, Valeriab | Colombo, Elenaa | Rossi, Paolo Dionigib | Mari, Danielaa; b
Affiliations: [a] Geriatric Unit, Department of Medical Sciences and Community Health, University of Milan, Milan, Italy | [b] Fondazione Ca’ Granda, IRCCS Ospedale Maggiore Policlinico, Milan, Italy | [c] Nutritional Sciences, University of Milan, Milan, Italy
Correspondence: [*] Correspondence to: Beatrice Arosio, Geriatric Unit, Department of Medical Sciences and Community Health, University of Milan, Via Pace 9, 20122 Milan, Italy. Tel.: +39 02 55035405; Fax: +39 02 50320735; E-mail: [email protected].
Abstract: As the European population gets older, the incidence of neurological disorders increases with significant impact on social costs. Despite differences in disease etiology, several brain disorders in the elderly (e.g., Alzheimer’s disease, vascular dementia, normal pressure hydrocephalus) share dementia as a common clinical feature. The current treatment for the majority of these diseases is merely symptomatic and does not modify the course of the illness. Symptoms of normal pressure hydrocephalus are the only ones that can be modified if they are recognized in time and treated appropriately. Therefore, an important clinical strategy may be disclosed by pathogenic pathways that can be modified and to find drugs that can slow down or even arrest disease progression. Possibly a way to answer this question could be by re-examining all the molecules which have so far succeeded in improving many aspects of cognitive deterioration in some neurodegenerative conditions, that were not considered because of controversial opinions. The main purpose of this summary is to further substantiate the hypothesis that the pathway of adenosine type A2A receptor could be used as a potential target to develop new/old therapeutic strategies.
Keywords: Adenosine, adenosine receptors, elderly, neurodegeneration
DOI: 10.3233/JAD-160324
Journal: Journal of Alzheimer's Disease, vol. 54, no. 2, pp. 417-425, 2016
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