Abstract：
:Chronic circadian disturbance, a condition of desynchronization between endogenous clock and environmental light-dark (LD) cycle, is known to cause adverse physiological changes including mortality. However, it is yet unclear whether these consequences result from disturbance of endogenous clock or condition of the LD cycle per se. To address this issue, we imposed 3 different periods of LD cycle (T) on wild type and functional clock-defective (Per1(-/-)Per2(-/-)) mice. We found that the disturbed rhythms of locomotor activity and body temperature resulted from interaction of endogenous clock and T cycle and the chronic state of the disturbance suppressed the endogenous circadian rhythm. Interestingly, the endogenous clock and the T cycles affected body weight and food intake independently, while their interaction affected the life span resulting increased mortality of wild type mice in a shortened T cycle. These results strongly indicate the presence of both separate and combined effects of the endogenous clock and T cycle on different physiological variables implying that shift work scheduling can be an important influence on health parameters.
journal_name
Neurobiol Agingjournal_title
Neurobiology of agingauthors
Park N,Cheon S,Son GH,Cho S,Kim Kdoi
10.1016/j.neurobiolaging.2011.11.005subject
Has Abstractpub_date
2012-06-01 00:00:00pages
1122.e11-22issue
6eissn
0197-4580issn
1558-1497pii
S0197-4580(11)00476-3journal_volume
33pub_type
杂志文章abstract：:It was previously reported that in soleus neuromuscular junctions of old mice, synaptic vesicle density was decreased while transmitter release was increased (compared to results in young mice). In the present study, two hypotheses that might resolve this disparity were tested. The first was that the density of readil...
journal_title：Neurobiology of aging
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更新日期：1987-01-01 00:00:00
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journal_title：Neurobiology of aging
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journal_title：Neurobiology of aging
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更新日期：2014-09-01 00:00:00
abstract：:Although important in neurodegeneration, systematic studies of nicotinic acetylcholine receptor expression in normal aging human brains are difficult to perform. We have studied the expression of nicotinic receptor alpha 4-1 and alpha 5 mRNA in the frontal and parietal isocortex of 3- (young adult), 24- (late middle a...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/s0197-4580(97)80316-8
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abstract：:While aged monkeys of several species show cerebral amyloid deposition in senile plaques and blood vessels similar to that seen in human aging and Alzheimer's disease (AD), studies of great apes have been limited. Using histological and immunohistochemical methods, we examined the brains of four orangutans aged 10, 28...
journal_title：Neurobiology of aging
pub_type： 杂志文章
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更新日期：1997-03-01 00:00:00
abstract：:We assessed whether polymers of N-acetylglucosamine (GlcNAc) have any pathogenetic role in Alzheimer's disease (AD). First, by using specific dyes, we found deposits of polymers of GlcNAc in sporadic but not in familial AD. We found that neurons and microglia exposed to GlcNAc and uridine diphosphate (UDP)-GlcNAc are ...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2014.12.033
更新日期：2015-05-01 00:00:00
abstract：:Estrogens have been implicated as possible therapeutic agents for improving cognition in postmenopausal women and have been linked to neurodegenerative disorders such as Alzheimer's disease. However, the utility of Premarin (Wyeth Pharmaceuticals, Markham, ON, Canada), a conjugated equine estrogen and the most commonl...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2012.07.009
更新日期：2013-03-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2009.05.005
更新日期：2011-05-01 00:00:00
abstract：:Modified forms of tau proteins are major components of the paired helical filaments (PHFs) present in Alzheimer brains. In this study, tau from cytosolic samples obtained from normal and Alzheimer disease brains were fractionated by iron-chelated affinity chromatography (ICAC) to discriminate between isoforms phosphor...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/0197-4580(95)00075-p
更新日期：1995-07-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2018.01.007
更新日期：2018-06-01 00:00:00
abstract：:We recently, characterized a novel peptide of the egg-laying controlling caudodorsal cells (CDC) of Lymnaea stagnalis. Here, we show that the novel peptide has autoinhibitory actions and its expression is significantly up-regulated in reproductively senescent animals. Intracellular recordings show that when bath-appli...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2005.03.020
更新日期：2006-05-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2015.12.002
更新日期：2016-03-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/0197-4580(89)90148-6
更新日期：1989-09-01 00:00:00
abstract：:Since estrogen is thought to protect pre-menopausal women from age-related hearing loss, we investigated whether variation in estrogen-signalling genes is linked to hearing status in the 1958 British Birth Cohort. This analysis implicated the estrogen-related receptor gamma (ESRRG) gene in determining adult hearing fu...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2013.02.009
更新日期：2013-08-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/s0197-4580(01)00227-5
更新日期：2001-07-01 00:00:00
abstract：:The apolipoprotein E (ApoE) ε4 allele has consistently been established as an Alzheimer's disease (AD) risk factor, but its pathological contribution to AD is obscure. Certain butyrylcholinesterase (BuChE) polymorphisms together with the ApoE ε4 allele synergistically increase the risk of AD. In addition, AD risk fact...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2009.07.015
更新日期：2011-07-01 00:00:00
abstract：:To better understand the role of insulin signaling in the development of Alzheimer's disease (AD), we utilized an animal model (intracerebroventricular injection of streptozotocin-ic-streptozotocin (STZ)) that displays insulin resistance only in the brain and exhibits AD pathology. In this model, deficits in hippocamp...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2010.12.002
更新日期：2012-02-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2015.10.014
更新日期：2016-02-01 00:00:00
abstract：:Accumulating evidence suggests that the propagation of hyperphosphorylation of tau protein and the amyloid-β peptide can be mediated by extracellular vesicles (EVs) and be associated with the onset and the progression of Alzheimer's disease (AD). As EVs may transfer between the brain and the blood, we have thus hypoth...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2019.10.010
更新日期：2020-02-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
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更新日期：1990-05-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2014.05.023
更新日期：2014-11-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2010.10.013
更新日期：2012-02-01 00:00:00
abstract：:Age-related differences in opiate receptors were determined using young (1 month old), mature (3 and 8 months old) and aged (20 months old) mice. 3H-Dihydromorphine binding to mu-receptors in brain synaptic membranes consisted of two components: one with high affinity and one with low affinity. High affinity mu bindin...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/s0197-4580(88)80066-6
更新日期：1988-05-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2007.07.010
更新日期：2009-03-01 00:00:00
abstract：:A major goal of animal research is to identify interventions that can promote successful aging and delay or reverse age-related cognitive decline in humans. Recent advances in standardizing cognitive assessment tools for humans have the potential to bring preclinical work closer to human research in aging and Alzheime...
journal_title：Neurobiology of aging
pub_type： 杂志文章,评审
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更新日期：2013-07-01 00:00:00
abstract：:RACK1 (receptor for activated C-kinase 1), an anchoring protein that shuttles activated PKC to cellular membranes, plays an important role in PKC-mediated signal transduction pathways. A significant loss of RACK1 has been found in the brain of aging animals and Alzheimer's disease (AD) patients, which implicates the p...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2009.10.017
更新日期：2011-10-01 00:00:00
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journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/0197-4580(89)90024-9
更新日期：1989-03-01 00:00:00
abstract：:Mutations in the presenilin genes account for the majority of familial Alzheimer disease (FAD) cases. In the present report we demonstrated that the FAD-linked presenilin 2 mutations (PS2 M239I and T122R) alter cystatin C trafficking in mouse primary neurons reducing secretion of its glycosylated form. These mutations...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2006.01.007
更新日期：2007-03-01 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
更新日期：1999-03-01 00:00:00
abstract：:Age-related structural brain changes have been demonstrated repeatedly but data on the effect of gender on age-related structural brain changes are conflicting. Using high-resolution T1-weighted magnetic resonance imaging and voxel-based morphometry, we examined a population of 133 healthy adults (women, 73; men, 60; ...
journal_title：Neurobiology of aging
pub_type： 杂志文章
doi：10.1016/j.neurobiolaging.2007.05.016
更新日期：2009-01-01 00:00:00
