Abstract:
:Long-term dietary supplementation with resveratrol protects against cardiovascular disease, osteoporesis, and metabolic decline. This study determined how long-term dietary resveratrol treatment protects against retinal ganglion cell (RGC) dendrite loss after optic nerve injury and alters the resolution of the unfolded protein response. Associated changes in markers of endoplasmic reticulum stress in RGCs also were investigated. Young-adult Thy1-yellow fluorescent protein (YFP) and C57BL/6 mice received either control diet or diet containing resveratrol for approximately 1 year. Both groups then received optic nerve crush (ONC). Fluorescent RGC dendrites in the Thy1-YFP mice were imaged weekly for 4 weeks after ONC. There was progressive loss of dendrite length in all RGC types within the mice that received control diet. Resveratrol delayed loss of dendrite complexity and complete dendrite loss for most RGC types. However, there were variations in the rate of retraction among different RGC types. Three weeks after ONC, cytoplasmic binding immunoglobulin protein (BiP) suppression observed in control diet ganglion cell layer neurons was reversed in mice that received resveratrol, nuclear C/EBP homologous protein (CHOP) was near baseline in control diet eyes but was moderately increased by resveratrol; and increased nuclear X-box-binding protein-1 (XBP-1) observed in control diet eyes was reduced in eyes that received resveratrol to the same level as in control diet uncrushed eyes. These results indicate that protection of dendrites by resveratrol after ONC differs among RGC types and suggest that alterations in long-term expression of binding immunoglobulin protein, CHOP, and XBP-1 may contribute to the resveratrol-mediated protection of RGC dendrites after ONC.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Lindsey JD,Duong-Polk KX,Hammond D,Leung CK,Weinreb RNdoi
10.1016/j.neurobiolaging.2014.12.021subject
Has Abstractpub_date
2015-05-01 00:00:00pages
1969-81issue
5eissn
0197-4580issn
1558-1497pii
S0197-4580(14)00837-9journal_volume
36pub_type
杂志文章abstract::The overall goal was to identify patterns of brain atrophy associated with cognitive impairment and future cognitive decline in non-demented elders. Seventy-one participants were studied with structural MRI and neuropsychological testing at baseline and 1-year follow-up. Deformation-based morphometry was used to exami...
journal_title:Neurobiology of aging
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abstract::Here we report the relationship between age at onset, clinical course and genotype in a family with combined LRRK2 G2019S and Parkin exon 2 deletions. In the combined mutation carriers the age at onset and clinical course was highly variable and not always younger than in the carriers of LRRK2 G2019S mutations alone. ...
journal_title:Neurobiology of aging
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doi:10.1016/j.neurobiolaging.2008.05.030
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abstract::The brain mechanisms underlying the effect of intellectual enrichment may evolve along the normal aging Alzheimer's disease (AD) cognitive spectrum and may include both protective and compensatory mechanisms. We assessed the association between early intellectual enrichment (education, years) and average cortical flor...
journal_title:Neurobiology of aging
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abstract::The available published guidelines for the housing of rodents are reviewed, and assessments are made with regard to whether the data on which these guidelines are based appear to be sound. Ambient air temperature, relative humidity, lighting levels and photoperiods, sound levels, cage sizes, and ventilation rates are ...
journal_title:Neurobiology of aging
pub_type: 杂志文章,评审
doi:10.1016/0197-4580(91)90116-2
更新日期:1991-11-01 00:00:00
abstract::Pertinent animal models of age-related learning deficiencies are required to elucidate the mechanism of age-related learning deficiencies and to develop novel therapeutic drugs for age-related diseases such as learning defects. Among many strains of accelerated senescence prone, senescence-accelerated mouse (SAM), SAM...
journal_title:Neurobiology of aging
pub_type: 杂志文章,评审
doi:10.1016/s0197-4580(99)00006-8
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abstract::Age-related brain changes are widely documented. Because of differences in measurement methods and case selection, the reported effects of age on regional grey and white matter brain volumes, however, are much more pronounced and widespread in neuroimaging than in postmortem studies. Consequently, the magnitude of the...
journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2007.10.015
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abstract::Insomnia, daytime sleepiness, and nocturnal wandering, so common in the elderly, are caused largely by two specific pathophysiologic processes. Sleep apnea is a condition where respiration pauses during sleep, leading to arousal. Sleep apnea is due either to obstruction in the throat or failure of the central respirat...
journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/0197-4580(82)90021-5
更新日期:1982-01-01 00:00:00
abstract:BACKGROUND:Aging is a major risk factor for a variety of neurobiological diseases leading to variations of transcriptional expression in affected tissues. Reverse transcription of RNA followed by quantitative PCR is a powerful technique for detection and quantification of specific transcripts differentially expressed. ...
journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2008.05.023
更新日期:2010-04-01 00:00:00
abstract::There is an unmet need for markers that can stratify different forms and subtypes of dementia. Because of similarities in clinical presentation, it can be difficult to distinguish between Alzheimer's disease (AD) and frontotemporal dementia (FTD). Using a multiplex targeted proteomic LC-MS/MS platform, we aimed to ide...
journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2018.08.019
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journal_title:Neurobiology of aging
pub_type: 临床试验,杂志文章,随机对照试验
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更新日期:2018-10-01 00:00:00
abstract::The activity of beta-secretase (BACE1), the endo-protease essential for the production of amyloid beta (Abeta) peptides, is increased in brain of late-onset sporadic Alzheimer's disease (AD), and oxidative stress is the potential cause of this event. Oxidative stress up-regulates the expression and the activity of BAC...
journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2007.12.015
更新日期:2009-10-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2006.08.005
更新日期:2007-12-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2020.10.023
更新日期:2020-11-14 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2008.05.006
更新日期:2010-01-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2010.03.012
更新日期:2012-02-01 00:00:00
abstract::Mutations in triggering receptor expressed on myeloid cells 2 (TREM2), which has been proposed to regulate the inflammatory responses and the clearance of apoptotic neurons and/or amyloid-β, are genetically linked to increased risk for late-onset Alzheimer's disease (AD). Interestingly, a missense variant in TREM-like...
journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2016.03.004
更新日期:2016-06-01 00:00:00
abstract::The growth hormone (GH) response to the dopamine (DA) receptor agonist, apomorphine HCl (Apo) (0.5 mg SC) was studied in young and elderly normal subjects as well as in patients with dementia of the Alzheimer type (DAT) and controls matched for age, gender and Quetelet index. The GH response was significantly decrease...
journal_title:Neurobiology of aging
pub_type: 杂志文章,评审
doi:10.1016/0197-4580(89)90055-9
更新日期:1989-05-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2017.07.007
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2014.08.005
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2016.07.009
更新日期:2016-11-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/s0197-4580(02)00013-1
更新日期:2003-01-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2004.09.001
更新日期:2005-01-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2017.02.002
更新日期:2017-05-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2007.08.014
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2006.05.017
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journal_title:Neurobiology of aging
pub_type: 杂志文章
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2015.05.002
更新日期:2015-08-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/j.neurobiolaging.2010.09.006
更新日期:2012-01-01 00:00:00
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journal_title:Neurobiology of aging
pub_type: 杂志文章
doi:10.1016/0197-4580(95)02030-6
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