The Multifactorial Etiopathogenesis of Alzheimer’s Disease: Neuroinflammation as the Major Contributor

Article type: Short Communication

Authors: González, Andrea^{a; b; *} | Calfio, Camila^{a; b} | Lüttges, Valentina^{a; b} | González-Madrid, Antonia^{a; b} | Guzmán, Cristian^{a; b}

Affiliations: [a] International Center for Biomedicine (ICC), Santiago, Chile | [b] Laboratory of Neurosciences and Functional Medicine, Faculty of Science, University of Chile, Santiago, Chile

Correspondence: [*] Correspondence to: Andrea González, PhD, International Center for Biomedicine, Avenida Vitacura 3568, Of 511, Vitacura, Santiago, Chile. E-mail: [email protected].

Abstract: Alzheimer’s disease (AD) is the most common form of dementia in the elderly. AD is a multifactorial disease, affected by several factors including amyloid-β42 oligomers, self-assembled tau, microbiota molecules, etc. However, inflammatory components are critical to trigger AD. Neuroinflammatory pathology links glial activation by “damage signals” with tau hyperphosphorylation, as explained by the Neuroimmunomodulation Theory, discovered by the ICC laboratory. This theory elucidates the onset and progression of several degenerative diseases and concept of “multitarget” therapy. These studies led to the rationale to identify inflammatory targets for the action of bioactive molecules or drugs against AD.

Keywords: Alzheimer’s disease, anti-inflammatory agents, blood-brain barrier, immunomodulation, neuroinflammation, proinflammatory markers

DOI: 10.3233/JAD-230150

Journal: Journal of Alzheimer's Disease, vol. 94, no. 1, pp. 95-100, 2023