Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2013, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2013/940603
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Funding
- Canadian Institutes of Health Research(CIHR), Canada
- Fonds de la recherche en sante du QC (FRSQ), Quebec, Canada
- National Institute on Minority Health and Health Disparities from the National Institutes of Health [G12MD007591]
- Semmes Foundation
- FRSQ, Canada
- National Institute on Minority Health and Health Disparities [G12MD007591] Funding Source: NIH RePORTER
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Alzheimer's disease (AD) is defined by the concurrence of abnormal aggregates composed of phosphorylated tau protein and of abnormal cellular changes including neurite degeneration, loss of neurons, and loss of cognitive functions. While a number of mechanisms have been implicated in this complex disease, oxidative stress remains one of the earliest and strongest events related to disease progression. However, the mechanism that links oxidative stress and cognitive decline remains elusive. Here, we propose that phosphorylated tau protein could be playing the role of potential connector and, therefore, that a combined therapy involving antioxidants and check points for synaptic plasticity during early stages of the disease could become a viable therapeutic option for AD treatment.
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