Exercise, cognitive function, and aging

Barnes, Jill N.

doi:10.1152/advan.00101.2014

Cited by 240 publications

(193 citation statements)

References 58 publications

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“…Cognitive impairment is multifactorial, but a history of cigarete smoking, aging and educational level are recognized as major determinants [25,26]. The origin of the cerebral dysfunction COPD -An Update in Pathogenesis and Clinical Managementin patients with COPD is still unknown, assuming the interference of several pathological relays: hypoxemia, oxidative stress, systemic inlammation, smoking, comorbidities, vascularmediated brain pathology, neurotransmiter metabolism in the central nervous system (CNS), a decrease in physical functioning, genetic and epigenetic factors.…”

Section: Copd: Fundamental Pathophysiological Mechanisms Susceptible mentioning

confidence: 99%

Neurocognitive Impairment as Systemic Effects of COPD

Oancea¹,

Tudorache²,

Tudorache³

2018

COPD - An Update in Pathogenesis and Clinical Management

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Mild cognitive impairment (MCI), also known as incipient dementia, is characterized by the decline of cognitive function greater than expected for a certain age and educational level of the individual but not severe enough to interfere with their daily activities. However, this mild cognitive impairment afects several areas: visuospatial, memory, atention and luency and it is a signiicant concern because it decreases the quality of life and treatment adherence of these patients. On the other hand, evidence suggests that individuals with Chronic obstructive pulmonary disease (COPD) also present an important risk of falls: 46% of these patients experience a fall/year, sometimes with fatal consequences. Standard clinical balance measures can predict the risk of falls in this population. Moreover, increased inlammatory biomarkers are associated with the decrease of cognitive functions and a higher risk of falls in this population. Patients with COPD have a higher balance and cognitive impairment than their healthy peers Therefore, it is important to identify, assess and understand the relevance of these comorbidities in order to characterize the full clinical spectrum of COPD and adjust prevention strategies, given the devastating consequences of these problems.

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Section: Copd: Fundamental Pathophysiological Mechanisms Susceptible mentioning

confidence: 99%

Neurocognitive Impairment as Systemic Effects of COPD

Oancea¹,

Tudorache²,

Tudorache³

2018

COPD - An Update in Pathogenesis and Clinical Management

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“…It should be noted that although most studies indicate that antioxidants protect against oxidative stress and thus extend lifespan (Anisimov et al ., 2011; Niu et al ., 2013) and lead to enhanced exercise capacity (Ji et al ., 1998), recently some reports indicated that antioxidants have no beneficial effects on exercise or are even harmful in high concentrations (Selman et al ., 2013). In addition, although a number of studies have reported that exercise leads to increased longevity (Holloszy, 1998; Navarro et al ., 2004; Barnes, 2015), one study in mice is not in agreement (Garcia‐Valles et al ., 2013). However, the overwhelming preponderance of data in patients support the concept that exercise improves not only healthy lifespan, but also longevity, as it clearly is protective against cardiovascular disease, diabetes, and obesity, all of which are known to reduce lifespan.…”

Section: Discussionmentioning

confidence: 96%

Type 5 adenylyl cyclase disruption leads to enhanced exercise performance

et al. 2015

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SummaryThe most important physiological mechanism mediating enhanced exercise performance is increased sympathetic, beta adrenergic receptor (β‐AR), and adenylyl cyclase (AC) activity. This is the first report of decreased AC activity mediating increased exercise performance. We demonstrated that AC5 disruption, that is, knock out (KO) mice, a longevity model, increases exercise performance. Importantly for its relation to longevity, exercise was also improved in old AC5 KO. The mechanism resided in skeletal muscle rather than in the heart, as confirmed by cardiac‐ and skeletal muscle‐specific AC5 KO's, where exercise performance was no longer improved by the cardiac‐specific AC5 KO, but was by the skeletal muscle‐specific AC5 KO, and there was no difference in cardiac output during exercise in AC5 KO vs. WT. Mitochondrial biogenesis was a major mechanism mediating the enhanced exercise. SIRT1, FoxO3a, MEK, and the anti‐oxidant, MnSOD were upregulated in AC5 KO mice. The improved exercise in the AC5 KO was blocked with either a SIRT1 inhibitor, MEK inhibitor, or by mating the AC5 KO with MnSOD hetero KO mice, confirming the role of SIRT1, MEK, and oxidative stress mechanisms. The Caenorhabditis elegans worm AC5 ortholog, acy‐3 by RNAi, also improved fitness, mitochondrial function, antioxidant defense, and lifespan, attesting to the evolutionary conservation of this pathway. Thus, decreasing sympathetic signaling through loss of AC5 is not only a mechanism to improve exercise performance, but is also a mechanism to improve healthful aging, as exercise also protects against diabetes, obesity, and cardiovascular disease, which all limit healthful aging.

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“…The major determinants of cognitive impairment include a history of cigarette smoking, increasing age, and educational level. [7][8][9] Therefore, the inclusion of a matched comparison group, a major strength of this study, might rule out the effect of smoking, age, and education on cognitive functioning. Although we did not match for gender and IQ, there were no significant differences in gender between both groups, and Z-scores were adjusted for educational level, age, and gender.…”

Section: Methodological Considerationsmentioning

confidence: 99%

“…[1][2][3][4] The prevalence rates of general cognitive impairment in COPD vary widely, ranging from 5.5% in a large sample of adults with COPD, measured with the Mini-Mental State Examination (MMSE), 5 up to 77.0% in patients with both COPD and hypoxemia, measured with multiple cognitive tests. 6 Increasing age is the most significant determinant of cognitive impairment, 7 besides a history of tobacco smoking 8 and a low educational level. 9 Although the exact pathogenesis of cognitive impairment in COPD remains unknown, vascular-mediated brain pathology, oxidative stress, hypoxemia, systemic inflammation, and comorbidities are proposed pathways to cognitive impairment.…”

Section: Introductionmentioning

confidence: 99%