Association between Apolipoprotein E Gene Polymorphism and Alzheimer's Disease in an Iranian Population: A Meta-Analysis

Abyadeh, Morteza; Djafarian, Kurosh; Heydarinejad, Fatemeh; Alizadeh, Shahab; Shab-Bidar, Sakineh

doi:10.1007/s12031-019-01381-1

Cited by 27 publications

(23 citation statements)

References 37 publications

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“…Several studies suggest a function of insulin resistance in pathophysiology of AD [ 27 , 28 ]. The association of Apo E gene polymorphism; which has a regulatory role in lipid metabolism [ 29 ], with both the risk of developing AD and type 2 diabetes mellitus (T2DM) supports this line of research [ 6 , 30 ]. Diabetes is a risk factor for the development of dementia and the disease was shown to enhance cognitive decline in APOE2/ APOE3 , but not APOE4 genotypes.…”

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confidence: 93%

“…The clearance of Aβ may be affected by several reasons including environmental and genetic factors such as apolipoprotein E polymorphism (Apo E2/3/4). Apo E4 isoform in particular has been showed to be associated with decreased Aβ catabolism and increased risk of AD [ 6 ].…”

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confidence: 99%

“…The protein phosphorylation is regulated by several kinases and phosphatases, including glycogen synthase kinase-3 (GSK-3), casein kinase 1 (CK1), cyclin-dependent kinase 5 (cdk5), 5′ adenosine monophosphate-activated protein kinase (AMPK), microtubule affinity-regulating kinases (MARKs), protein phosphatase-1, 2A, and 5 (PP1, PP2A, and PP5)[ 22 - 24 ]. Abnormal hyperphosphorylation of tau (p-tau) affects its affinity to bind microtubules and leads to micro-tubular dysfunction, the enhanced cytosolic level of p-tau subsequently form NFTs [ 25 , 26 ] which are associated with axonal degeneration, synaptic dysfunction and neuronal loss in AD [ 6 , 21 ].…”

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confidence: 99%

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et al. 2021

Aging and disease

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confidence: 93%

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Comparative Analysis of Aducanumab, Zagotenemab and Pioglitazone as Targeted Treatment Strategies for Alzheimer’s Disease

Abyadeh

Gupta

et al. 2021

Aging and disease

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“…Alzheimer's disease (AD) is the leading cause of dementia, affecting between 70 to 80% of older adults with dementia [1]. Currently, over 50 million people are living with the disease worldwide, and this number is estimated to rise to 150 million in 2050, exacerbating an already constrained healthcare system unless preventive strategies are implemented [2,3]. AD is characterized by initial memory loss and learning impairment, followed by cognitive dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Key Genes and Biochemical Networks in Various Brain Regions Affected in Alzheimer’s Disease

Abyadeh

Tofigh

Hosseinian

et al. 2022

Cells

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Alzheimer’s disease (AD) is one of the most complicated progressive neurodegenerative brain disorders, affecting millions of people around the world. Ageing remains one of the strongest risk factors associated with the disease and the increasing trend of the ageing population globally has significantly increased the pressure on healthcare systems worldwide. The pathogenesis of AD is being extensively investigated, yet several unknown key components remain. Therefore, we aimed to extract new knowledge from existing data. Ten gene expression datasets from different brain regions including the hippocampus, cerebellum, entorhinal, frontal and temporal cortices of 820 AD cases and 626 healthy controls were analyzed using the robust rank aggregation (RRA) method. Our results returned 1713 robust differentially expressed genes (DEGs) between five brain regions of AD cases and healthy controls. Subsequent analysis revealed pathways that were altered in each brain region, of which the GABAergic synapse pathway and the retrograde endocannabinoid signaling pathway were shared between all AD affected brain regions except the cerebellum, which is relatively less sensitive to the effects of AD. Furthermore, we obtained common robust DEGs between these two pathways and predicted three miRNAs as potential candidates targeting these genes; hsa-mir-17-5p, hsa-mir-106a-5p and hsa-mir-373-3p. Three transcription factors (TFs) were also identified as the potential upstream regulators of the robust DEGs; ELK-1, GATA1 and GATA2. Our results provide the foundation for further research investigating the role of these pathways in AD pathogenesis, and potential application of these miRNAs and TFs as therapeutic and diagnostic targets.

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“…Было высказано предположение, что распространенность БА выше у женщин по сравнению с мужчинами [10]. Аполипопротеин В4 (Apolipoprotein E4, ApoE4) также относится к факторам риска развития БА, и было показано, что женщины -носительницы аллеля ApoE4 имеют более высокий риск развития данного заболевания [10,11].…”

Section: роль оксидативного стресса в развитии болезни альцгеймераunclassified

The role of oxidative stress in the development of Alzheimer's disease

Nikolenko

Rizaeva

Bulygin

et al. 2022

RJTAO

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Болезнь Альцгеймера (БА), описанная в 1907 г. немецким психиатром Алоисом Альцгеймером, представляет собой прогрессирующее нейродегенеративное заболевание, характеризующееся потерей памяти, когнитивными и поведенческими нарушениями, которые в конечном итоге приводят к деменции [1]. В возникновении БА могут играть роль как генетические, так и экологические факторы риска, но самым большим фактором риска является возраст: в 65 лет вероятность развития БА составляет около 3%, а к 85 годам она возрастает до более чем 30% [2, 3]. В 2015 г. во всем мире БА страдали 23-35 млн человек. Кроме того, по оценкам, к 2050 г. из-за старения населения распространенность БА возрастет до 106,8 млн [4]. Клинические проявления БА возникают в результате дисфункции и гибели нейронов, особенно в тех популяциях нервных клеток, которые отвечают за память и познание [5]. Предполагается, что патофизиологический процесс инициируется внеклеточным фибриллярным отложением бета-амилоида (Aβ) с последующей внутринейрональной гиперфосфорилированной агрегацией тау-белка [5, 6].В настоящее время выделяют две формы БА. Первая форма (также известная как наследственная форма БА, НФБА) встречается примерно в 1-5% всех случаев, диагностированных как БА [7]. Она характеризуется ранним началом (до 65 лет) и часто связана с мутациями в гене белкапредшественника амилоида (amyloid precursor protein, APP) и генах пресенелина-1 (presenilin-1, PS-1) или пресенелина-2 (presenilin-2, PS-2) -компонентов комплекса гамма-О Б З О Р Ы

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Association between Apolipoprotein E Gene Polymorphism and Alzheimer's Disease in an Iranian Population: A Meta-Analysis

Cited by 27 publications

References 37 publications

Comparative Analysis of Aducanumab, Zagotenemab and Pioglitazone as Targeted Treatment Strategies for Alzheimer’s Disease

Comparative Analysis of Aducanumab, Zagotenemab and Pioglitazone as Targeted Treatment Strategies for Alzheimer’s Disease

Key Genes and Biochemical Networks in Various Brain Regions Affected in Alzheimer’s Disease

The role of oxidative stress in the development of Alzheimer's disease

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