The association of apolipoprotein E (ApoE) genotype and cognitive outcomes in multiple sclerosis; a systematic review and meta-analysis

Naseri, Amirreza; Baghernezhad, Kosar; Seyedi‐Sahebari, Sepideh; Alhoseini, Seyed Ardalan; Gholipour-khalili, Elnaz; Zafarani, Fatemeh; Talebi, Mahnaz

doi:10.1016/j.msard.2022.104011

Cited by 13 publications

(2 citation statements)

References 49 publications

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“…APOE-ε4 may be associated with the onset and progression of cognitive impairment in patients with MS. Individuals with MS and APOE-ε4 experienced delayed rates to stimuli and difficulties with cognitive function [164]. In patients with optic neuritis [165,166], a common occurrence in almost half of patents with MS. APOE serum levels were significantly higher than in control patient groups and the APOE ε3/ε3 genotype may increase the risk of developing optic neuritis in males [167].…”

Section: Cognitive Loss and Dementia That Can Occur In Multiple Scler...mentioning

confidence: 99%

Cognitive Impairment in Multiple Sclerosis

Maiese

2023

Bioengineering

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Almost three million individuals suffer from multiple sclerosis (MS) throughout the world, a demyelinating disease in the nervous system with increased prevalence over the last five decades, and is now being recognized as one significant etiology of cognitive loss and dementia. Presently, disease modifying therapies can limit the rate of relapse and potentially reduce brain volume loss in patients with MS, but unfortunately cannot prevent disease progression or the onset of cognitive disability. Innovative strategies are therefore required to address areas of inflammation, immune cell activation, and cell survival that involve novel pathways of programmed cell death, mammalian forkhead transcription factors (FoxOs), the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), and associated pathways with the apolipoprotein E (APOE-ε4) gene and severe acute respiratory syndrome coronavirus (SARS-CoV-2). These pathways are intertwined at multiple levels and can involve metabolic oversight with cellular metabolism dependent upon nicotinamide adenine dinucleotide (NAD+). Insight into the mechanisms of these pathways can provide new avenues of discovery for the therapeutic treatment of dementia and loss in cognition that occurs during MS.

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Section: Cognitive Loss and Dementia That Can Occur In Multiple Scler...mentioning

confidence: 99%

Cognitive Impairment in Multiple Sclerosis

Maiese

2023

Bioengineering

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“…At least sixty-five percent of patients with MS have difficulty with memory recall and executive ability (252). Cognitive loss in MS patients may be tied to metabolic pathways and APOE-ϵ4 since individuals with MS can demonstrate lower cognitive function and delayed responses to stimuli (368). APOE serum levels are elevated in individuals with demyelinating optic neuritis and the genotype of APOE ϵ3/ϵ3 may lead to the male onset of optic neuritis (327).…”

Section: The Clinical Onset Of Metabolic Mediated Neurodegenerative D...mentioning

confidence: 99%

The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk

Maiese

2023

Front. Immunol.

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Life expectancy is increasing throughout the world and coincides with a rise in non-communicable diseases (NCDs), especially for metabolic disease that includes diabetes mellitus (DM) and neurodegenerative disorders. The debilitating effects of metabolic disorders influence the entire body and significantly affect the nervous system impacting greater than one billion people with disability in the peripheral nervous system as well as with cognitive loss, now the seventh leading cause of death worldwide. Metabolic disorders, such as DM, and neurologic disease remain a significant challenge for the treatment and care of individuals since present therapies may limit symptoms but do not halt overall disease progression. These clinical challenges to address the interplay between metabolic and neurodegenerative disorders warrant innovative strategies that can focus upon the underlying mechanisms of aging-related disorders, oxidative stress, cell senescence, and cell death. Programmed cell death pathways that involve autophagy, apoptosis, ferroptosis, and pyroptosis can play a critical role in metabolic and neurodegenerative disorders and oversee processes that include insulin resistance, β-cell function, mitochondrial integrity, reactive oxygen species release, and inflammatory cell activation. The silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), AMP activated protein kinase (AMPK), and Wnt1 inducible signaling pathway protein 1 (WISP1) are novel targets that can oversee programmed cell death pathways tied to β-nicotinamide adenine dinucleotide (NAD+), nicotinamide, apolipoprotein E (APOE), severe acute respiratory syndrome (SARS-CoV-2) exposure with coronavirus disease 2019 (COVID-19), and trophic factors, such as erythropoietin (EPO). The pathways of programmed cell death, SIRT1, AMPK, and WISP1 offer exciting prospects for maintaining metabolic homeostasis and nervous system function that can be compromised during aging-related disorders and lead to cognitive impairment, but these pathways have dual roles in determining the ultimate fate of cells and organ systems that warrant thoughtful insight into complex autofeedback mechanisms.

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Cognitive impairment in multiple sclerosis: from phenomenology to neurobiological mechanisms

Jellinger

2024

J Neural Transm

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The association of apolipoprotein E (ApoE) genotype and cognitive outcomes in multiple sclerosis; a systematic review and meta-analysis

Cited by 13 publications

References 49 publications

Cognitive Impairment in Multiple Sclerosis

Cognitive Impairment in Multiple Sclerosis

The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk

Cognitive impairment in multiple sclerosis: from phenomenology to neurobiological mechanisms

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