Exercise alters the immune profile in Tg2576 Alzheimer mice toward a response coincident with improved cognitive performance and decreased amyloid

Nichol, Kathryn; Poon, Wayne W.; Parachikova, Anna; Cribbs, David H.; Glabe, Charles G.; Cotman, Carl W.

doi:10.1186/1742-2094-5-13

Cited by 209 publications

(138 citation statements)

References 75 publications

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“…34 The addition of new cells requires increased nutrients, which are supplied by new vasculature. 35 In a mouse model of AD, exercising animals show a reduction in ␤-amyloid deposits, 36 reduced tau formation, 37 and superior learning rates compared to sedentary animals. 38 Our results are encouraging, but need to be interpreted in light of some important limitations.…”

Section: Resultsmentioning

confidence: 99%

Physical activity predicts gray matter volume in late adulthood

Erickson

Raji²,

López³

et al. 2010

Neurology

436

336

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Objectives: Physical activity (PA) has been hypothesized to spare gray matter volume in late adulthood, but longitudinal data testing an association has been lacking. Here we tested whether PA would be associated with greater gray matter volume after a 9-year follow-up, a threshold could be identified for the amount of walking necessary to spare gray matter volume, and greater gray matter volume associated with PA would be associated with a reduced risk for cognitive impairment 13 years after the PA evaluation. Methods:In 299 adults (mean age 78 years) from the Cardiovascular Health Cognition Study, we examined the association between gray matter volume, PA, and cognitive impairment. Physical activity was quantified as the number of blocks walked over 1 week. High-resolution brain scans were acquired 9 years after the PA assessment on cognitively normal adults. White matter hyperintensities, ventricular grade, and other health variables at baseline were used as covariates. Clinical adjudication for cognitive impairment occurred 13 years after baseline.

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Section: Resultsmentioning

confidence: 99%

Physical activity predicts gray matter volume in late adulthood

Erickson

Raji²,

López³

et al. 2010

Neurology

436

336

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“…This has been the subject of many prior reviews and, therefore, will not be discussed at length (Brody and Holtzman 2008;Hawkes and McLaurin 2007;Maier et al 2005;Morgan 2006;Okura and Matsumoto 2007;Schenk et al 2005;Steinitz 2008). However, several recent rodent studies have either attempted to directly modulate microglial phenotype or have concluded that changes in microglial phenotype contribute to altered plaque load or inflammatory state in the brain independent of any active or passive vaccination strategy (Ding et al 2008;El Khoury et al 2007;Jiang et al 2008;Jin et al 2008;Maier et al 2008;Nichol et al 2008;Richard et al 2008;Scholtzova et al 2009;Shaftel et al 2007;Town et al 2008). It is important to note that, these studies, in line with the immunization approaches, have directly or indirectly sought to alter microglial behavior rather than generally inhibit it.…”

Section: Modulating Microglial Phenotype To Improve Disease Conditionmentioning

confidence: 99%

Inflammation and Microglia Actions in Alzheimer’s Disease

Combs

2009

J Neuroimmune Pharmacol

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A variety of studies have documented increased presence of reactive microglia in the brains of not only Alzheimer's disease (AD) patients but its transgenic mouse models. Since these cells are often characterized in association with fibrillar Abeta peptide-containing plaques, it has been assumed that plaque interaction provides one stimulus for the phenotype observed. The growing appreciation that microglia phenotype changes with age and that resident immune cells are commingled with blood-derived macrophage has complicated understanding of the behavior of these cells in AD. In addition, comparison of microglia within AD brains and the many rodent models suggests that there are population phenotype differences among these cells within any given brain during disease. Recent immunomodulatory strategies that have been employed, although effective at improving behavioral performance, decreasing Abeta plaque load, and altering immune molecule levels, have not yet resolved the details and dynamics of the microglial and macrophage responses. The heterogeneity of microglial presentation in AD brains and its transgenic mouse models and the outcomes of immunoregulatory efforts will be reviewed below along with the remaining question of how much understanding of microglial behavior is actually required in order to propose a microglia-related therapy for AD.

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“…With regard to neurodegenerative diseases (e.g., MCI or AD), several non-human animal studies also found that aerobic exercise could decrease brain amyloid burden and pathogenic phenotypes, facilitate neuronal survivability and function modulated by BDNF, and improve cognitive performance in a transgenic mouse model of AD [85][86][87][88]. Recently, Baker et al [48] found that long-term aerobic exercise could effectively improve multiple tests of executive control (e.g., task switching) for individuals with aMCI, and suggested that such an exercise mode plays a protective role by attenuating progression of cognitive symptoms in aMCI, although the beneficial effects of exercise on cognitive functions were more pronounced for the aMCI women than aMCI men, despite comparable gains in cardiorespiratory fitness.…”

Section: Discussionmentioning

confidence: 99%

The Role of Physical Fitness in the Neurocognitive Performance of Task Switching in Older Persons with Mild Cognitive Impairment

Tsai

Pai

Ukropec

et al. 2016

JAD

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Abstract. Although elderly people with amnestic mild cognitive impairment (aMCI) have been found to show impaired behavioral performance in task switching, no research has yet explored the electrophysiological mechanisms and the potential correlation between physical fitness and neurocognitive (i.e., behavioral and electrophysiological) performance in aMCI. The present study was thus aimed to examine whether there are differences in electrophysiological (i.e., event-related potential) performance between aMCI participants and controls when performing a task-switching paradigm, and to investigate the role of physical fitness in the relationship between neurocognitive performance and aMCI. Sixty participants were classified into aMCI (n = 30) and control (n = 30) groups, and performed a task-switching paradigm with concomitant electrophysiological recording, as well as underwent senior functional physical fitness tests. The aMCI group showed comparable scores on most parts of the physical fitness tests, but reduced lower body flexibility and VO 2max as compared to the control group. When performing the task-switching paradigm, the aMCI group showed slower reaction times in the heterogeneous condition and larger global switching costs, although no significant difference was observed in accuracy rates between the two groups. In addition, the aMCI group showed significantly prolonged P3 latencies in the homogeneous and heterogeneous conditions, and a smaller P3 amplitude only in the heterogeneous condition. The level of cardiorespiratory fitness was significantly correlated with P3 amplitude in the aMCI group, particularly in the heterogeneous condition of the task-switching paradigm. These results show that the aMCI group exhibited abnormalities in their neurocognitive performance when performing the task-switching paradigm and such a deficit was likely associated with reduced cardiorespiratory fitness, which was shown to be the important predictor of neurocognitive performance.

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Exercise alters the immune profile in Tg2576 Alzheimer mice toward a response coincident with improved cognitive performance and decreased amyloid

Cited by 209 publications

References 75 publications

Physical activity predicts gray matter volume in late adulthood

Physical activity predicts gray matter volume in late adulthood

Inflammation and Microglia Actions in Alzheimer’s Disease

The Role of Physical Fitness in the Neurocognitive Performance of Task Switching in Older Persons with Mild Cognitive Impairment

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