Epigenetic Determinants of Healthy and Diseased Brain Aging and Cognition

Akbarian, Schahram; Beeri, Michal Schnaider; Haroutunian, Vahram

doi:10.1001/jamaneurol.2013.1459

Cited by 73 publications

(52 citation statements)

References 92 publications

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“…Indeed, aged mice with learning and memory impairments demonstrate hypoacetylation of H4K12; restoration of H4K12 acetylation by using histone deacetylase (HDAC) inhibitors ameliorates the memory deficits [181,182]. Epigenetic changes associated with aging have also been observed on other acetylated sites [183]. …”

Section: Aging and Epigeneticsmentioning

confidence: 99%

“…Studies of DNA methylation indicate that aged rats with learning and memory impairments display abnormal methylation of memory promoting genes [186]. Identified sites include H3K36me3, H4K20me1, H3K9me2/3, and H3K27me3 [183]. A recent study demonstrated that increased expression of DNA methyl transferase 3a2 (DNMT3a2) can rescue age-related memory impairment in aged mice.…”

Section: Aging and Epigeneticsmentioning

confidence: 99%

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Molecular and cellular aspects of age-related cognitive decline and Alzheimer’s disease

Hullinger

Puglielli

2017

Behavioural Brain Research

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As the population of people aged 60 or older continues to rise, it has become increasingly important to understand the molecular basis underlying age-related cognitive decline. In fact, a better understanding of aging biology will help us identify ways to maintain high levels of cognitive functioning throughout the aging process. Many cellular and molecular aspects of brain aging are shared with other organ systems; however, certain age-related changes are unique to the nervous system due to its structural, cellular and molecular complexity. Importantly, the brain appears to show differential changes throughout the aging process, with certain regions (e.g. frontal and temporal regions) being more vulnerable than others (e.g. brain stem). Within the medial temporal lobe, the hippocampus is especially susceptible to age-related changes. The important role of the hippocampus in age-related cognitive decline and in vulnerability to disease processes such as Alzheimer’s disease has prompted this review, which will focus on the complexity of changes that characterize aging, and on the molecular connections that exist between normal aging and Alzheimer’s disease. Finally, it will discuss behavioral interventions and emerging insights for promoting healthy cognitive aging.

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Section: Aging and Epigeneticsmentioning

confidence: 99%

Section: Aging and Epigeneticsmentioning

confidence: 99%

Molecular and cellular aspects of age-related cognitive decline and Alzheimer’s disease

Hullinger

Puglielli

2017

Behavioural Brain Research

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“…methylation of CpG dinucleotide islands, which are usually found in proximity to (or within) promoters. Although some genes become hypermethylated over time, there is a trend towards global loss of DNA methylation (hypomethylation) throughout life (Gonzalo, 2010), a trend that may be a contributory factor in age related neurodegenerative disorders (Akbarian et al, 2013; Johnson et al, 2012). The importance of DNA methylation in the regulation of gene expression is further demonstrated by the fact that hypermethylation and hypomethylation, relative to normal tissue, have been implicated in a variety of human cancers where, typically, there is hypermethylation of tumor suppressor genes and hypomethylation of oncogenes (Gokul and Khosla, 2013).…”

Section: What Is the Neuroepigenome And Why Is It Important?mentioning

confidence: 99%

Understanding the genetic liability to schizophrenia through the neuroepigenome

Fullard

Halene

Giambartolomei

et al. 2016

Schizophrenia Research

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The Psychiatric Genomics Consortium-Schizophrenia Workgroup (PGC-SCZ) recently identified 108 loci associated with increased risk for schizophrenia (SCZ). The vast majority of these variants reside within non-coding sequences of the genome and are predicted to exert their effects by affecting the mechanism of action of cis regulatory elements (CREs), such as promoters and enhancers. Although a number of large-scale collaborative efforts (e.g. ENCODE) have achieved a comprehensive mapping of CREs in human cell lines or tissue homogenates, it is becoming increasingly evident that many risk-associated variants are enriched for expression Quantitative Trait Loci (eQTLs) and CREs in specific tissues or cells. As such, data derived from previous research endeavors may not capture fully cell-type and/or region specific changes associated with brain diseases. Coupling recent technological advances in genomics with cell-type specific methodologies, we are presented with an unprecedented opportunity to better understand the genetics of normal brain development and function and, in turn, the molecular basis of neuropsychiatric disorders. In this review, we will outline ongoing efforts towards this goal and will discuss approaches with the potential to shed light on the mechanism(s) of action of cell-type specific cis regulatory elements and their putative roles in disease, with particular emphasis on understanding the manner in which the epigenome and CREs influence the etiology of SCZ.

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“…Idosos que participam de programas de atividade física (caminhada, fortalecimento muscular, resistência, flexibilidade e equilíbrio) apresentam melhor qualidade de vida do que idosos que não participam dessas atividades (25) . No tocante ao grau de instrução na população idosa, é importante destacar o fato de que a escolaridade apresenta associação com a cognição, visto que o baixo nível de escolaridade tem relação direta com difusão, ou perda cognitiva (26) . A escolaridade constitui-se um dos principais aspectos relacionados à qualidade de vida em diferentes grupos populacionais.…”

Section: Discussionunclassified