Oxidative stress, an imbalance of pro-oxidants and antioxidants, is linked to aging and many neurological disorders such as Alzheimer's disease, the most common form of dementia. In the recent years, a number of scientific publications have reported that PPARs, a group of nuclear receptor proteins controlling gene activity within our body, play an important role at normal and pathological levels in different tissues, including the nervous tissue. In fact, their involvement in neurodegenerative diseases, such as multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer's, Parkinson's and Huntington's diseases, is well recognized.
More, 4-HNE, a substance that initiates a physiological response when combined with one type of PPARs molecules, namely PPARβ/δ, is known to be involved in neurodegenerative diseases as well. Now, a new study from the Sbarro Health Research Organization and the University of L'Aquila (Italy) has investigated the role of 4-HNE and PPAR β/δ during AD progression and in physiological aging.
The data obtained using a special AD animal model, indicate a novel destructive age-dependent role of PPAR β/δ in AD. This finding just published on Cell Cycle, may have important implications for the prevention of cognitive impairment in elderly and in neurodegenerative diseases.
"Our studies point towards the possibility to use a specific PPARβ/δ antagonist for counteracting the disease progression" says Annamaria Cimini of the University of L'Aquila, lead author of the study. "Understanding the mechanism of action of physiological and pathological aging may provide a means to limit cognitive impairment progression" says Antonio Giordano, founder and President of the Sbarro Health Research Organization.
The abstract to the article is available at: https://www.landesbioscience.com/journals/cc/article/28295/
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