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Common Pathological Mechanisms and Risk Factors for Alzheimer's Disease and Type-2 Diabetes: Focus on Inflammation

Moyse, Emmanuel, Haddad, Mohamed, Benlabiod, Camelia, Ramassamy, Charles ORCID: https://orcid.org/0000-0002-3252-5878 et Krantic, Slavica (2019). Common Pathological Mechanisms and Risk Factors for Alzheimer's Disease and Type-2 Diabetes: Focus on Inflammation Current Alzheimer Research , vol. 16 , nº 11. p. 986-1006. DOI: 10.2174/1567205016666191106094356.

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Résumé

BACKGROUND: Diabetes is considered as a risk factor for Alzheimer's disease, but it is yet un-clear whether this pathological link is reciprocal. Although Alzheimer's disease and diabetes appear as entirely different pathological entities affecting the central nervous system and a peripheral organ (pan-creas), respectively, they share a common pathological core. Recent evidence suggests that in the pancreas in the case of diabetes, as in the brain for Alzheimer's disease, the initial pathological event may be the accumulation of toxic proteins yielding amyloidosis. Moreover, in both pathologies, amyloidosis is likely responsible for local inflammation, which acts as a driving force for cell death and tissue degeneration. These pathological events are all inter-connected and establish a vicious cycle resulting in the progressive character of both pathologies.

OBJECTIVE: To address the literature supporting the hypothesis of a common pathological core for both diseases.

DISCUSSION: We will focus on the obvious differences between the disease-related inflammatory changes in a peripheral organ, such as the pancreas, versus those observed in the brain. Recent evidence suggesting an impact of peripheral inflammation on neuroinflammation in Alzheimer's disease will be presented.

CONCLUSION: We propose that it is now necessary to consider whether neuroinflammation in Alzheimer's disease affects inflammation in the pancreas related to diabetes.

Type de document: Article
Mots-clés libres: Amyloidosis; advanced glycation end products; cytokines; hyperglycemia; innate immune response; insulin resistance; microglia; vasculopathy
Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 22 juill. 2021 21:51
Dernière modification: 15 févr. 2022 21:24
URI: https://espace.inrs.ca/id/eprint/11644

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