Cognitive dysfunction with aging and the role of inflammation

Simen, Arthur A.; Bordner, Kelly A.; Martin, Mark P.; Moy, Lawrence A.; Barry, Lisa C.

doi:10.1177/2040622311399145

Cited by 157 publications

(155 citation statements)

References 214 publications

(267 reference statements)

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“…The balancing and stress-reducing effects of MM may positively influence ageing by improving functioning of ANS ), HPA axis and immune functions (Creswell et al 2012;Epel et al 2009;Epel et al 2013;Larouche et al 2015). As all three factors have been implicated in decline of brain structure (Frewen et al 2013;Larouche et al 2015;Lupien et al 2009;McEwen and Magarinos 2001;Simen et al 2011), the brain state training of MM may also enhance neural reserve via this indirect pathway.…”

Section: Ageing Lifestyle and Cognitive Reservementioning

confidence: 99%

Meditation and Cognitive Ageing: the Role of Mindfulness Meditation in Building Cognitive Reserve

Malinowski

Shalamanova

2017

J Cogn Enhanc

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Mindfulness-related meditation practices engage various cognitive skills including the ability to focus and sustain attention, which in itself requires several interacting attentional subfunctions. There is increasing behavioural and neuroscientific evidence that mindfulness meditation improves these functions and associated neural processes. More so than other cognitive training programmes, the effects of meditation appear to generalise to other cognitive tasks, thus demonstrating far transfer effects. As these attentional functions have been linked to age-related cognitive decline, there is growing interest in the question whether meditation can slowdown or even prevent such decline. The cognitive reserve hypothesis builds on evidence that various lifestyle factors can lead to better cognitive performance in older age than would be predicted by the existing degree of brain pathology. We argue that mindfulness meditation, as a combination of brain network and brain state training, may increase cognitive reserve capacity and may mitigate age-related declines in cognitive functions. We consider available direct and indirect evidence from the perspective of cognitive reserve theory. The limited available evidence suggests that MM may enhance cognitive reserve capacity directly through the repeated activation of attentional functions and of the multiple demand system and indirectly through the improvement of physiological mechanisms associated with stress and immune function. The article concludes with outlining research strategies for addressing underlying empirical questions in more substantial ways.

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Section: Ageing Lifestyle and Cognitive Reservementioning

confidence: 99%

Meditation and Cognitive Ageing: the Role of Mindfulness Meditation in Building Cognitive Reserve

Malinowski

Shalamanova

2017

J Cogn Enhanc

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“…First, we cannot determine causality, because this study was cross-sectional. However, prior studies have provided evidence that inflammation has a role in the progression of cognitive impairment [46,47]. These findings give us confidence that inflammation influences cognition during HAND, rather than the reverse.…”

Section: Discussionmentioning

confidence: 67%

Monocyte Activation Is Associated With Worse Cognitive Performance in HIV-Infected Women With Virologic Suppression

et al. 2016

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Background. Cognitive impairment persists despite suppression of plasma human immunodeficiency virus (HIV) RNA. Monocyte-related immune activation is a likely mechanism. We examined immune activation and cognition in a cohort of HIVinfected and uninfected women from the Women's Interagency HIV Study (WIHS).Methods. Blood levels of activation markers, soluble CD163 (sCD163), soluble CD14 (sCD14), CRP, IL-6, and a gut microbial translocation marker (intestinal fatty acid binding protein (I-FABP)) were measured in 253 women (73% HIV-infected). Markers were compared to concurrent (within ± one semiannual visit) neuropsychological testing performance.Results. Higher sCD163 levels were associated with worse overall performance and worse verbal learning, verbal memory, executive function, psychomotor speed, and fine motor skills (P < .05 for all comparisons). Higher sCD14 levels were associated with worse verbal learning, verbal memory, executive function, and psychomotor speed (P < .05 for all comparisons). Among women with virological suppression, sCD163 remained associated with overall performance, verbal memory, psychomotor speed, and fine motor skills, and sCD164 remained associated with executive function (P < .05 for all comparisons). CRP, IL-6, and I-FABP were not associated with worse cognitive performance.Conclusions. Monocyte activation was associated with worse cognitive performance, and associations persisted despite viral suppression. Persistent inflammatory mechanisms related to monocytes correlate to clinically pertinent brain outcomes.Keywords. CD163; CD14; women; HIV infection; cognition disorders; intesticial fatty acid-binding protein (1-19).Human immunodeficiency virus (HIV)-associated neurocognitive disorder (HAND) is a debilitating condition that affects up to 50% of people living with HIV, despite access to combination antiretroviral therapy (cART) [1]. Understanding the cellular and molecular mechanisms leading to HAND is of clinical importance, particularly among those adherent to treatment, as HAND is associated with loss of employment [2], decreased ability to multitask [3], impaired medication self-management [4], and shorter time to virologic failure.[5] These factors influence health and quality of life [6]. Chronic immune activation is a common theme in describing potential mechanisms underlying persistence of HAND despite suppression of plasma viremia [7]. Two postulated sources of this immune activation are intracellular HIV DNA in tissues and circulating cells (eg, monocytes, lymph nodes, and, potentially, the brain) and gut microbial translocation [8,9]. However, published work describing HAND is frequently based on the evaluation of study participants who have a mixture of suppressed or unsuppressed plasma HIV RNA levels, a factor that limits our understanding of persistent impairment despite suppressive therapy [10].Circulation of activated CD14 + /CD16 + monocytes containing HIV contribute to chronic immune activation. These monocytes are theorized to carry HIV into the brain [7]....

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“…Additionally, prolonged allograft ischemic time has been associated with impaired gas exchange (i.e., Pa O 2 /FI O 2 ) immediately postoperatively (34) and impaired longterm survival. Confirmatory studies, designed to examine markers of oxidative stress (34,35), inflammation (e.g., IL-18) (35,(43)(44)(45), and oxygenation postoperatively as potential mediators of the observed relationships between allograft ischemic time, oxygenation, and cognitive function, are required to validate our observations. Related future studies are required to examine whether the previously identified relationship between prolonged allograft ischemic time and long-term survival (34) is mediated by cognitive impairment and the potential adverse events related to such impairment (i.e., functional impairment, medication nonadherence, infectious complications) (46,47).…”

Section: Original Researchmentioning

confidence: 85%

“…We had proposed that allograft ischemic time may result in cognitive decline due to systemic effects of ischemia-reperfusion injury, mediated by oxidative stress and inflammation, which could lead to neuroinflammation (34,35,43,44). Additionally, prolonged allograft ischemic time has been associated with impaired gas exchange (i.e., Pa O 2 /FI O 2 ) immediately postoperatively (34) and impaired longterm survival.…”

Section: Original Researchmentioning

confidence: 99%

Cognitive Function, Mental Health, and Health-related Quality of Life after Lung Transplantation

Cohen

Christie²,

Anderson³

et al. 2014

Annals ATS

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Rationale: Cognitive and psychiatric impairments are threats to functional independence, general health, and quality of life. Evidence regarding these outcomes after lung transplantation is limited.Objectives: Determine the frequency of cognitive and psychiatric impairment after lung transplantation and identify potential factors associated with cognitive impairment after lung transplantation.Methods: In a retrospective cohort study, we assessed cognitive function, mental health, and health-related quality of life using a validated battery of standardized tests in 42 subjects posttransplantation. The battery assessed cognition, depression, anxiety, resilience, and post-traumatic stress disorder (PTSD). Cognitive function was assessed using the Montreal Cognitive Assessment, a validated screening test with a range of 0 to 30. We hypothesized that cognitive function post-transplantation would be associated with type of transplant, cardiopulmonary bypass, primary graft dysfunction, allograft ischemic time, and physical therapy posttransplantation. We used multivariable linear regression to examine the relationship between candidate risk factors and cognitive function post-transplantation.Measurements and Main Results: Mild cognitive impairment (score, 18-25) was observed in 67% of post-transplant subjects (95% confidence interval [CI]: 50-80%) and moderate cognitive impairment (score, 10-17) was observed in 5% (95% CI, 1-16%) of post-transplant subjects. Symptoms of moderate to severe anxiety and depression were observed in 21 and 3% of post-transplant subjects, respectively. No transplant recipients reported symptoms of PTSD. Higher resilience correlated with less psychological distress in the domains of depression (P , 0.001) and PTSD (P = 0.02). Prolonged graft ischemic time was independently associated with worse cognitive performance after lung transplantation (P = 0.001).The functional gain in 6-minute-walk distance achieved at the end of post-transplant physical rehabilitation (P = 0.04) was independently associated with improved cognitive performance post-transplantation.Conclusions: Mild cognitive impairment was present in the majority of patients after lung transplantation. Prolonged allograft ischemic time may be associated with cognitive impairment. Poor physical performance and cognitive impairment are linked, and physical rehabilitation post-transplant and psychological resilience may be protective against the development of long-term impairment. Further study is warranted to confirm these potential associations and to examine the trajectory of cognitive function after lung transplantation.Keywords: lung transplantation; cognitive function; psychological function; quality of life; critical illness

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Cognitive dysfunction with aging and the role of inflammation

Cited by 157 publications

References 214 publications

Meditation and Cognitive Ageing: the Role of Mindfulness Meditation in Building Cognitive Reserve

Meditation and Cognitive Ageing: the Role of Mindfulness Meditation in Building Cognitive Reserve

Monocyte Activation Is Associated With Worse Cognitive Performance in HIV-Infected Women With Virologic Suppression

Cognitive Function, Mental Health, and Health-related Quality of Life after Lung Transplantation

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