Inflammation as a Possible Link Between Dyslipidemia and Alzheimer’s Disease

Oliveira, Bruno Cabral de Lima; Bellozi, Paula Maria Quaglio; Reis, Helton José; Oliveira, Antônio Carlos Pinheiro de

doi:10.1016/j.neuroscience.2018.02.012

Cited by 28 publications

(17 citation statements)

References 222 publications

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“…Inflammation is a compelling candidate mechanism by which several genetic and environmental factors have been linked with AD risk. Systemic and neural inflammation are implicated as key components in the development and progression of AD pathogenesis (32,58,59). Because obesity induces elevated inflammation in brain and peripheral tissues (31,60,61), inflammatory pathways have been implicated in mediating obesity-related AD risk (62).…”

Section: Discussionmentioning

confidence: 99%

APOEgenotype affects metabolic and Alzheimer‐related outcomes induced by Western diet in female EFAD mice

Christensen

Pike

2018

FASEB j.

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Development of Alzheimer's disease (AD) is regulated by interactive effects of genetic and environmental risk factors. The most significant genetic risk factor for AD is the ε4 allele of apolipoprotein E (APOE4), which has been shown to exert greater AD risk in women. An important modifiable AD risk factor is obesity and its associated metabolic dysfunctions. Whether APOE genotype might interact with obesity in females to regulate AD pathogenesis is unclear. To investigate this issue, we studied the effects of Western diet (WD) on female EFAD mice, a transgenic mouse model of AD that includes human APOE alleles ε3 (E3FAD) and ε4 (E4FAD). EFAD mice were fed either control (10% fat, 7% sugar) or WD (45% fat, 17% sugar), and both metabolic and neuropathologic outcomes were determined. Although E4FAD mice generally exhibited poorer metabolic status at baseline, E3FAD mice showed greater diet‐induced metabolic impairments. Similarly, E4FAD mice exhibited higher levels of AD‐related pathology overall, but only E3FAD showed significant increases on select measures of β‐amyloid pathology after exposure to WD. These data demonstrate a gene–environment interaction between APOE and obesogenic diets in females. Understanding how AD‐promoting effects of obesity are modulated by genetic factors will foster the identification of at‐risk populations and development of preventive interventions.—Christensen, A., Pike, C. J. APOE genotype affects metabolic and Alzheimer‐related outcomes induced by Western diet in female EFAD mice. FASEB J. 33, 4054–4066 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

APOEgenotype affects metabolic and Alzheimer‐related outcomes induced by Western diet in female EFAD mice

Christensen

Pike

2018

FASEB j.

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“…It is synthesized in astrocytes and macrophages, and it is the most abundant apolipoprotein in the CNS. Research indicates that genetically determined changes in the amino acid sequence of APOE can lead to Aβ accumulation, exacerbate its neurotoxic effects, and increase neuroinflammation [4,18]. There are three different alleles encoding APOE: ε2, ε3, and ε4.…”

Section: Genetic Factorsmentioning

confidence: 99%

“…It accounts for 60%-80% of all cases of dementia, which is the fifth leading cause of death worldwide [2,3]. AD affects primarily the elderly population and is becoming a global health concern; in 2015, 47 million people suffered from dementia, and this number is estimated to reach 131 million in 2050 [4]. Currently, there are no effective therapies to stop or reverse the disease; therefore, a lot of studies are focused on preventive methods for AD.…”

Section: Introductionmentioning

confidence: 99%

The Role of Selected Bioactive Compounds in the Prevention of Alzheimer’s Disease

Grodzicki

Dziendzikowska

2020

Antioxidants

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Neurodegeneration is a feature of many debilitating, incurable age-dependent diseases that affect the nervous system and represent a major threat to the health of elderly persons. Because of the ongoing process of aging experienced by modern societies, the increasing prevalence of neurodegenerative diseases is becoming a global public health concern. A major cause of age-related dementia is Alzheimer’s disease (AD). Currently, there are no effective therapies to slow, stop, or reverse the progression of this disease. However, many studies have suggested that modification of lifestyle factors, such as the introduction of an appropriate diet, can delay or prevent the onset of this disorder. Diet is currently considered to be a crucial factor in controlling health and protecting oneself against oxidative stress and chronic inflammation, and thus against chronic degenerative diseases. A large number of bioactive food compounds may influence the pathological mechanisms underlying AD. Among them, phenolic compounds, omega-3 fatty acids, fat-soluble vitamins, isothiocyanates, and carotenoids seem to be promising. They act not only as antioxidant and anti-inflammatory agents, but also as active modulators of the pathological molecular mechanisms that play a role in AD development, including the formation of amyloid plaques and tau tangles, the main hallmarks of AD pathology. In vivo animal model studies as well as clinical and epidemiological research suggest that nutritional intervention has a positive effect on the health of older people and may prevent age-related cognitive decline, especially when the diet contains more than one bioactive nutrient. The Mediterranean diet and in particular its combination with Dietary Approaches to Stop Hypertension, which is called the MIND diet, are nutritional patterns based on many products rich in bioactive compounds that appear to be the most effective in preventing neurodegeneration. The present review gathers evidence that supports the neuroprotective effect of bioactive substances.

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“…Notably, most of these factors are relevant to inflammation and immunity. Consequently, a variety of hypotheses and theories of AD have been proposed, among which the inflammation hypothesis is receiving growing support (Newcombe et al, 2018; Oliveira et al, 2018; Schultzberg et al, 2018; Spangenberg and Green, 2018). Although the reviews of neuroinflammation and AD are abundant and comprehensive (for more detail, we recommend Ref; Josef Karkos, 2003; Heppner Frank et al, 2015; Ransohoff, 2016; Cuello, 2017), we will focus on the relationship between microglia and neuroinflammation because microglia harbor the majority of CCR5 in the CNS.…”

Section: Ad and Neuroinflammationmentioning

confidence: 99%

Entanglement of CCR5 and Alzheimer’s Disease

Zhu

2019

Front. Aging Neurosci.

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Although the mechanisms of Alzheimer’s disease are diverse and unclear, the past 20 years have witnessed the unprecedented development of the AD inflammation theory. As a key inflammatory receptor family, the C-C chemokine receptor family is a remarkable participant in the cause of Alzheimer’s disease; of this family, CCR5 is the most widely studied. CCR5 is an essential entrance when HIV infects immune cells and is also involved in other inflammatory and immune activities. New evidence on the inevitably intertwined link between Alzheimer’s disease and CCR5 indicates that CCR5 accelerates the development of Alzheimer’s disease, and few studies disputed it. The role of CCR5 in Alzheimer’s disease remains elusive. However, as the research progresses, this intricate relationship will gradually be uncovered.

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Inflammation as a Possible Link Between Dyslipidemia and Alzheimer’s Disease

Cited by 28 publications

References 222 publications

APOEgenotype affects metabolic and Alzheimer‐related outcomes induced by Western diet in female EFAD mice

APOEgenotype affects metabolic and Alzheimer‐related outcomes induced by Western diet in female EFAD mice

The Role of Selected Bioactive Compounds in the Prevention of Alzheimer’s Disease

Entanglement of CCR5 and Alzheimer’s Disease

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