Oxidative Stress in Alzheimer’s Disease: Should We Keep Trying Antioxidant Therapies?. Ferreira, M. E. S., Vasconcelos, A. S. d., Vilhena, T. d. C., Silva, T. L. d., Barbosa, A. d. S., Gomes, A. R. Q., Dolabela, M. F., & Percário, S. Cellular and Molecular Neurobiology, 35(5):595–614, July, 2015. Paper doi abstract bibtex The risk of chronic diseases such as Alzheimer’s disease is growing as a result of the continuous increasing average life span of the world population, a syndrome characterized by the presence of intraneural neurofibrillary tangles and senile plaques composed mainly by beta-amyloid protein, changes that may cause a number of progressive disorders in the elderly, causing, in its most advanced stage, difficulty in performing normal daily activities, among other manifestations. Therefore, it is important to understand the underlying pathogenic mechanisms of this syndrome. Nevertheless, despite intensive effort to access the physiopathological pathways of the disease, it remains poorly understood. In that context, some hypotheses have arisen, including the recent oxidative stress hypothesis, theory supported by the involvement of oxidative stress in aging, and the vulnerability of neurons to oxidative attack. In the present revision, oxidative changes and redox mechanisms in Alzheimer’s disease will be further stressed, as well as the grounds for antioxidant supplementation as adjuvant therapy for the disease will be addressed.
@article{ferreira_oxidative_2015,
title = {Oxidative {Stress} in {Alzheimer}’s {Disease}: {Should} {We} {Keep} {Trying} {Antioxidant} {Therapies}?},
volume = {35},
issn = {0272-4340, 1573-6830},
shorttitle = {Oxidative {Stress} in {Alzheimer}’s {Disease}},
url = {http://link.springer.com/article/10.1007/s10571-015-0157-y},
doi = {10.1007/s10571-015-0157-y},
abstract = {The risk of chronic diseases such as Alzheimer’s disease is growing as a result of the continuous increasing average life span of the world population, a syndrome characterized by the presence of intraneural neurofibrillary tangles and senile plaques composed mainly by beta-amyloid protein, changes that may cause a number of progressive disorders in the elderly, causing, in its most advanced stage, difficulty in performing normal daily activities, among other manifestations. Therefore, it is important to understand the underlying pathogenic mechanisms of this syndrome. Nevertheless, despite intensive effort to access the physiopathological pathways of the disease, it remains poorly understood. In that context, some hypotheses have arisen, including the recent oxidative stress hypothesis, theory supported by the involvement of oxidative stress in aging, and the vulnerability of neurons to oxidative attack. In the present revision, oxidative changes and redox mechanisms in Alzheimer’s disease will be further stressed, as well as the grounds for antioxidant supplementation as adjuvant therapy for the disease will be addressed.},
language = {en},
number = {5},
urldate = {2016-11-10TZ},
journal = {Cellular and Molecular Neurobiology},
author = {Ferreira, Michelli Erica Souza and Vasconcelos, Amanda Soares de and Vilhena, Thyago da Costa and Silva, Thiago Leite da and Barbosa, Aline da Silva and Gomes, Antonio Rafael Quadros and Dolabela, Maria Fani and Percário, Sandro},
month = jul,
year = {2015},
pages = {595--614}
}
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