Alzheimer’s disease (AD) is the main cause of dementia. Multiple physiopathological mechanisms are postulated to explain cognitive deterioration: Aβ toxicity, cholinergic dysfunction, Tau alterations, oxidative damage, synaptic dysfunction and secondary inflammation to plaques. In the laboratory of Neuroscience, we propose that inflammation and cell stress associated with ageing participate in the development of AD, whose central pathogenic event would involve glial dysfunction.

 The association of neuroinflammation with AD is supported by neuropathological and epidemiological studies. However, it remains unknown whether inflammation is a cause or a consequence of the neurodegenerative process. Inflammation facilitates defective processing of beta-amyloid (Aβ) and amyloid precursor protein (APP), enabling Aβ-aggregation but also modifying Aβ-reactivity.
We have observed that microglial reactivity to APP and Aβ is low, but it is exacerbated in pro-inflammatory conditions, showing that citotoxicity could depend on inflammatory capacitating of glia. We propose that Aβ-accumulation, oxidative stress, synaptic dysfunction and neurodegeneration depend on the inflammatory status of the nervous system, which triggers the deregulation of glial activation.

The results derived from the laboratory of Neuroscience support our hypothesis that inflammation is both a trigger of Aβ-accumulation and one of the main causes of neurodegeneration in AD. The glia dysfunctional response, besides being cause of AD, is likely to participate in the pathogeny of other neurodegenerative diseases.




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