Histone deacetylase gene variants predict brain volume changes in multiple sclerosis

Inkster, Becky; Strijbis, Eva; Vounou, Maria; Kappos, Ludwig; Radue, Ernst‐Wilhelm; Matthews, Paul M.; Uitdehaag, Bernard M. J.; Barkhof, Frederik; Polman, Chris H.; Montana, Giovanni; Geurts, Jeroen J. G.

doi:10.1016/j.neurobiolaging.2012.07.007

Cited by 30 publications

(19 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These data reduction methods boost the power and efficiency of the search when all predictors are weak. Even so, they often make effective predictions when aggregated 37 .…”

Section: Tactics To Reduce the Search Spacementioning

confidence: 99%

Whole-genome analyses of whole-brain data: working within an expanded search space

et al. 2014

View full text Add to dashboard Cite

Large-scale comparisons of patients and healthy controls have unearthed genetic risk factors associated with a range of neurological and psychiatric illnesses. Meanwhile, brain imaging studies are increasing in size and scope, revealing disease and genetic effects on brain structure and function, and implicating neural pathways and causal mechanisms. With the advent of global neuroimaging consortia, imaging studies are now well powered to discover genetic variants that reliably affect the brain. Genetic analyses of brain measures from tens of thousands of people are being extended to test genetic associations with signals at millions of locations in the brain. Connectome-wide, genome-wide scans can jointly screen brain circuits and genomes, presenting new statistical challenges. There is a growing need for the community to establish and enforce standards in this developing field to ensure robust findings. Here we discuss how neuroimagers and geneticists have formed alliances to discover how genetic factors affect the brain. The field is rapidly advancing with ultra-high-resolution imaging and whole-genome sequencing. We recommend a rigorous approach to neuroimaging genomics that capitalizes on its recent successes and ensures the reliability of future discoveries.

show abstract

“…These data reduction methods boost the power and efficiency of the search when all predictors are weak. Even so, they often make effective predictions when aggregated 37 .…”

Section: Tactics To Reduce the Search Spacementioning

confidence: 99%

Whole-genome analyses of whole-brain data: working within an expanded search space

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Epigenetics is involved in various brain related disorders and physiologic responses that genetics alone does not completely explain including AD, depression, schizophrenia, glioma, addiction, Rett syndrome, alcohol dependence, autism, epilepsy, multiple sclerosis and stress (Heim & Binder, 2012; Inkster et al, 2013; Jaenisch & Bird, 2003; Kreth et al, 2012; Maric & Svrakic, 2012; Maze & Nestler, 2011; Mifsud et al, 2011; Nguyen et al, 2010; Orr et al, 2012; Qureshi & Mehler, 2010; Shahbazian & Zoghbi, 2002; Taqi et al, 2011; Zawia et al, 2009). As neurons do not divide and cannot be replaced after degeneration, epigenetic changes resulting in neuronal dysfunction need to be targeted and modified to prevent neurodegeneration (Bird, 2007; Selvi et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Epigenetics: A novel therapeutic approach for the treatment of Alzheimer's disease

Adwan

Zawia

2013

Pharmacology & Therapeutics

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is the most common type of dementia in the elderly. It is characterized by the deposition of two forms of aggregates within the brain, the amyloid β plaques and tau neurofibrillary tangles. Currently, no disease-modifying agent is approved for the treatment of AD. Approved pharmacotherapies target the peripheral symptoms but they do not prevent or slow down the progression of the disease. Although several disease-modifying immunotherapeutic agents are in clinical development, many have failed due to lack of efficacy or serious adverse events. Epigenetic changes including DNA methylation and histone modifications are involved in learning and memory and have been recently highlighted for holding promise as potential targets for AD therapeutics. Dynamic and latent epigenetic alterations are incorporated in AD pathological pathways and present valuable reversible targets for AD and other neurological disorders. The approval of epigenetic drugs for cancer treatment has opened the door for the development of epigenetic drugs for other disorders including neurodegenerative diseases. In particular, methyl donors and histone deacetylase inhibitors are being investigated for possible therapeutic effects to rescue memory and cognitive decline found in such disorders. This review explores the area of epigenetics for potential AD interventions and presents the most recent findings in this field.

show abstract

“…Human-MS Decrease of SIRT1 expression in PBMCs in Relapse phase (Ciriello et al, 2018;Hewes et al, 2017;Tegla et al, 2014) Human-MS Increase of SIRT1 expression in acute and chronic lesion sites (Tegla et al, 2014) Human-MS Increase of SIRT1 level in plasma samples (Pennisi et al, 2011) SIRT2 Wistar rats RNA knockdown of SIRT2 Increase of tubulin acetylation, MBP expression, and cell arbor complexity of OPCs (Li et al, 2007) Human-MS Presence of antibodies against SIRT2 in the CSF (Lovato et al, 2008) EAE mouse Decrease in the level of SIRT2 (Jastorff et al, 2009) EAE mouse Increase in level of transcription of SIRT2 in the CNS during chronic disease stages (Prozorovski et al, 2019) Human-MS Decrease in level of several isoform of SIRT2 in MS lesions (Jastorff et al, 2009) SIRT3 Human-MS Reduction in the level of SIRT3 expression in MS affected brain (Rice et al, 2012) SIRT4 Human-MS Change in genetic variants (Inkster et al, 2013) SIRT5 Human-MS Change in genetic variants (Inkster et al, 2013) SIRT6 EAE mouse Increase in level of transcription of SIRT6 in the CNS during chronic disease stages (Prozorovski et al, 2019) SIRT7 EAE mouse…”

Section: Sirtuin-1mentioning

confidence: 99%

Sirtuins in Multiple Sclerosis: The crossroad of neurodegeneration, autoimmunity and metabolism

Foolad

Khodagholi

Javan

2019

Multiple Sclerosis and Related Disorders

View full text Add to dashboard Cite

Histone deacetylase gene variants predict brain volume changes in multiple sclerosis

Cited by 30 publications

References 66 publications

Whole-genome analyses of whole-brain data: working within an expanded search space

Whole-genome analyses of whole-brain data: working within an expanded search space

Epigenetics: A novel therapeutic approach for the treatment of Alzheimer's disease

Sirtuins in Multiple Sclerosis: The crossroad of neurodegeneration, autoimmunity and metabolism

Contact Info

Product

Resources

About