Affiliations: [a] Laboratory of Cellular and Molecular Neurosciences, Faculty of Sciences, University of Chile, Santiago, Chile
| [b]
International Center for Biomedicine (ICC), Santiago, Chile
| [c] Department of Neurological Sciences East, Faculty of Medicine, University of Chile, Santiago, Chile
Correspondence:
[*]
Correspondence to: Dr. Ricardo B. Maccioni, International Center for Biomedicine, Vitacura 3568, D513, Vitacura, Chile. E-mail: rmaccion@manquehue.net.
Abstract: Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a progressive cognitive impairment of patients, affecting around 12% of people older than 65 years old. WHO estimated that over 48.6 million all over the world suffer this disease. On the basis of cumulative results on our research, we have postulated the neuroimmunomodulation hypothesis that appears to provide a reasonable explanation of both the preclinical and clinical observations. In this context, the long-term activation of the innate immune system triggers an anomalous cascade of molecular signals, finally leading to tau oligomerization in the pathway to neuronal degeneration. In the present scenario of the failure of many anti-AD drugs, nutraceutical compounds provide an avenue for AD prevention and possibly as coadjuvants in the treatment of this disease. Recent discoveries point to the relevance of curcumin, a natural anti-inflammatory agent, in controlling oxidative stress and improving cholinergic function in the brain, even though the mechanisms underlying these actions are unknown. We investigated the effects of curcumin in cultures of neuronal cells. For this study, we exposed cells to prooxidant conditions, both in the presence and absence of curcumin. Our data reveal that curcumin exert a strong neuroprotective effect in N2a cells, thus preventing toxicity by oxidative agents H2O2 and Fe+3. This is supported by results that indicate that curcumin control the neurodegenerative effects of both oxidative agents, relieving cells from the loss of neuritogenic processes induced by prooxidants. In addition, curcumin was able to slow down the tau aggregation curve and disassemble tau pathological oligomeric structures. Data suggest that curcumin could be a potential compound for prevention of cognitive disorders associated with AD.
Keywords: Alzheimer’s disease, curcumin and derivatives, functional effects in neurons, prevention, treatment
