Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration

Dijk, Gertjan van; Heijningen, Steffen van; Reijne, Aaffien C.; Nyakas, Csaba; Zee, Eddy A. van der; Eisel, Ulrich

doi:10.3389/fnins.2015.00173

Cited by 63 publications

(43 citation statements)

References 289 publications

(334 reference statements)

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“…Metabolic syndrome affects cognitive performance, including memory, executive function, processing speed, and overall intellectual capabilities [23, 49–52]. The adverse effect of metabolic syndrome on cognitive function suggests that it may be associated with an increased risk of developing AD [50–52]. Notably, the prevalence of metabolic syndrome is the highest among Latino adults, suggesting that it could be a risk factor that may contribute to health disparities in AD.…”

Section: Epidemiology Of Ad In the Latino Populationmentioning

confidence: 99%

Alzheimer’s Disease in the Latino Community: Intersection of Genetics and Social Determinants of Health

Vega

Cabrera

Wygant

et al. 2017

JAD

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Alzheimer’s disease (AD) is the most common type of dementia among individuals 65 or older. There are more than 5 million diagnosed cases in the US alone and this number is expected to triple by 2050. Therefore, AD has reached epidemic proportions with significant socioeconomic implications. While aging in general is the greatest risk factor for AD, several additional demographic factors that have contributed to the rise in AD in the US are under study. One such factor is associated with the relatively fast growth of the Latino population. Several reports indicate that AD is more prevalent among blacks and Latinos. However, the reason for AD disparity among different ethnic groups is still poorly understood and highly controversial. The Latino population is composed of different groups based on nationality, namely South and Central America, Mexico, and Caribbean Hispanics. This diversity among the Latino population represents an additional challenge since there are distinct characteristics associated with AD and comorbidities. In this review, we aim to bring attention to the intersection between social determinants of health and genetic factors associated with AD within the Latino community. We argue that understanding the interplay between identified social determinants of health, co-morbidities, and genetic factors could lead to community empowerment and inclusiveness in research and healthcare services, contributing to improved diagnosis and treatment of AD patients. Lastly, we propose that inserting a neuroethics perspective could help understand key challenges that influence healthcare disparities and contribute to increased risk of AD among Latinos.

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Section: Epidemiology Of Ad In the Latino Populationmentioning

confidence: 99%

Alzheimer’s Disease in the Latino Community: Intersection of Genetics and Social Determinants of Health

Vega

Cabrera

Wygant

et al. 2017

JAD

View full text Add to dashboard Cite

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“…The mechanism by which this toxicity in the brain occurs is still unknown; however, neuroinflammation, particularly priming of the brain’s resident immune cells, microglia, resulting in both detrimental and protective functions under pathological conditions, as measured by cytokine production, may underlie several cognitive and neurodegenerative disorders [16]. Additionally, chronic systemic inflammation resulting from cardiovascular disease (CVD) may be associated with an increased risk for developing neuroinflammation potentially leading to neurodegenerative disorders [17]. …”

Section: Introductionmentioning

confidence: 99%

Surface area-dependence of gas-particle interactions influences pulmonary and neuroinflammatory outcomes

et al. 2016

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BackgroundDeleterious consequences of exposure to traffic emissions may derive from interactions between carbonaceous particulate matter (PM) and gaseous components in a manner that is dependent on the surface area or complexity of the particles. To determine the validity of this hypothesis, we examined pulmonary and neurological inflammatory outcomes in C57BL/6 and apolipoprotein E knockout (ApoE−/−) male mice after acute and chronic exposure to vehicle engine-derived particulate matter, generated as ultrafine (UFP) and fine (FP) sizes, with additional exposures using UFP or FP combined with gaseous copollutants derived from fresh gasoline and diesel emissions, labeled as UFP + G and FP + G.ResultsThe UFP and UFP + G exposure groups resulted in the most profound pulmonary and neuroinflammatory effects. Phagocytosis of UFP + G particles via resident alveolar macrophages was substantial in both mouse strains, particularly after chronic exposure, with concurrent increased proinflammatory cytokine expression of CXCL1 and TNFα in the bronchial lavage fluid. In the acute exposure paradigm, only UFP and UFP + G induced significant changes in pulmonary inflammation and only in the ApoE−/− animals. Similarly, acute exposure to UFP and UFP + G increased the expression of several cytokines in the hippocampus of ApoE−/− mice including Il-1β, IL-6, Tgf-β and Tnf-α and in the hippocampus of C57BL/6 mice including Ccl5, Cxcl1, Il-1β, and Tnf-α. Interestingly, Il-6 and Tgf-β expression were decreased in the C57BL/6 hippocampus after acute exposure. Chronic exposure to UFP + G increased expression of Ccl5, Cxcl1, Il-6, and Tgf-β in the ApoE−/− hippocampus, but this effect was minimal in the C57BL/6 mice, suggesting compensatory mechanisms to manage neuroinflammation in this strain.ConclusionsInflammatory responses the lung and brain were most substantial in ApoE−/− animals exposed to UFP + G, suggesting that the surface area-dependent interaction of gases and particles is an important determinant of toxic responses. As such, freshly generated UFP, in the presence of combustion-derived gas phase pollutants, may be a greater health hazard than would be predicted from PM concentration, alone, lending support for epidemiological findings of adverse neurological outcomes associated with roadway proximity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0177-x) contains supplementary material, which is available to authorized users.

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“…Many epidemiological studies suggest that metabolic dysfunction increases the risk for Alzheimer's disease (AD) and its prodrome, mild cognitive impairment (MCI) [1,2]. Whilst the exact mechanisms are unclear, conditions such as type 2 diabetes, insulin resistance and metabolic syndrome (MetS) predict AD neuropathology in late-onset patients [3,4] and late middle-aged adults at risk for AD [5]. Despite growing interest in metabolic dysfunction and AD, the effects of MetS and related factors on cognition and especially affect are not well studied.…”

mentioning

confidence: 99%

Does metabolic syndrome impact cognition and emotion in Alzheimer's disease?

Willette

2015

Euro J of Neurology

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Integrative neurobiology of metabolic diseases, neuroinflammation, and neurodegeneration

Cited by 63 publications

References 289 publications

Alzheimer’s Disease in the Latino Community: Intersection of Genetics and Social Determinants of Health

Alzheimer’s Disease in the Latino Community: Intersection of Genetics and Social Determinants of Health

Surface area-dependence of gas-particle interactions influences pulmonary and neuroinflammatory outcomes

Does metabolic syndrome impact cognition and emotion in Alzheimer's disease?

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