Abstract:
:Alzheimer's disease (AD) is a devastating age-related neurodegenerative disease with no specific treatment at present. Several healthy lifestyle options and over-the-counter drugs that it has been suggested delay the onset of the disease are in an experimental phase, but it is unclear whether they will have any therapeutic value against AD. We assayed physical exercise and melatonin in 3xTg-AD male mice aged from 6 to 12 months, therefore from moderate to advanced phases of AD pathology. Analysis of behavior and brain tissue at termination showed differential patterns of neuroprotection for the 2 treatments. Both treatments decreased soluble amyloid β oligomers, whereas only melatonin decreased hyperphosphorylated tau. Melatonin was effective against the immunosenescence that 3xTg-AD mice present. Voluntary physical exercise protected against behavioral and psychological symptoms of dementia such as anxiety, a lack of exploration, and emotionality. Both treatments protected against cognitive impairment, brain oxidative stress, and a decrease in mitochondrial DNA (mtDNA). Interestingly, only the combined treatment of physical exercise plus melatonin was effective against the decrease of mitochondrial complexes. Therefore, melatonin plus physical exercise may exert complementary, additive, or even synergistic effects against a range of disturbances present in AD.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
García-Mesa Y,Giménez-Llort L,López LC,Venegas C,Cristòfol R,Escames G,Acuña-Castroviejo D,Sanfeliu Cdoi
10.1016/j.neurobiolaging.2011.11.016subject
Has Abstractpub_date
2012-06-01 00:00:00pages
1124.e13-29issue
6eissn
0197-4580issn
1558-1497pii
S0197-4580(11)00495-7journal_volume
33pub_type
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
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