79 results match your criteria: "National Institutes on Aging[Affiliation]"

Context: Subclinical thyroid dysfunction (ScTD) comprising subclinical hypothyroidism (SHypo) and subclinical hyperthyroidism (SHyper) has been associated with increased risk for cardiovascular events.

Objective: To assess associations between ScTD and cardiovascular risk factors (cvRFs) according to age and sex.

Design And Setting: Pooled individual participant data analysis of large prospective cohort studies from the Thyroid Studies Collaboration.

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Article Synopsis
  • Iron is a vital mineral connected to various biological functions, with studies linking its dysregulation to cardiovascular and neurodegenerative diseases, though the cause-effect relationship remains unclear.
  • The research utilized computational methods and meta-analysis of genome-wide studies to look at how genetically predicted iron levels relate to the risk of 11 different diseases, revealing significant correlations especially with coronary heart disease and cholesterol levels.
  • The findings suggest a potential protective effect of iron on Parkinson's disease risk in women, highlighting the need for further exploration of how iron impacts health differently across sexes and could inform future disease prevention and treatment strategies.
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Article Synopsis
  • Many studies on brain diseases mostly involve people of European descent, which makes it hard to understand these diseases for everyone.
  • Out of 123 studies, 82% mainly included European participants, finding many genetic markers, while only a few were found in studies with non-European participants.
  • It’s super important to include more diverse backgrounds in future research to improve treatments and knowledge about these brain diseases.
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India is a large middle-income country and has surpassed China in overall population, comprising 20% of the global population (over 1.43 billion people). India is experiencing a major demographic shift in its aging population.

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Article Synopsis
  • Many genetic studies about brain diseases mostly include participants of European ancestry, which is a problem for understanding these diseases better for everyone.
  • The goal of the research was to see how many participants from different backgrounds were included in studies about neurodegenerative diseases and to find out if that affects the results.
  • The findings showed that 82% of these studies were mainly European, and studies including non-European participants identified much fewer risk factors compared to the European-focused studies.
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Although growth/differentiation factor 11 (GDF11), growth/differentiation factor 8 (GDF8), and their circulating antagonists, which include GDF11 and GDF8 propeptides, follistatin (FST), WAP, Follistatin/Kazal, Immunoglobulin, Kunitz And Netrin Domain Containing (WFIKKN)1, and WFIKKN2, have been shown to influence skeletal muscle and aging in mice, the relationship of these circulating factors with human phenotypes is less clear. This study aimed to characterize the relationship between plasma GDF8, GDF11, FST, WFIKKN1, and WFIKKN2 concentrations with the decline of grip strength in 534 adults, ≥65 years, who participated in the Baltimore Longitudinal Study of Aging and had grip strength measured over time. Plasma GDF8 and GDF11 mature proteins, GDF8 and GDF11 propeptides, FST (isoform FST315 and cleaved form FST303), WFIKKN1, and WFIKKN2 concentrations were measured using selected reaction monitoring-tandem mass spectrometry at baseline.

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Math-anxious people consistently underperform in math. The most widely accepted explanation for why this underperformance occurs is that math-anxious people experience heightened anxiety when faced with math, and this in-the-moment anxiety interferes with performance. Surprisingly, this explanation has not been tested directly.

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Introduction: Racial disparities in dementia incidence exist, but less is known about their presence and drivers among middle-aged adults.

Methods: We used time-to-event analysis among a sample of 4378 respondents (age 40-59 years at baseline) drawn from the third National Health and Nutrition Examination Surveys (NHANES III) with administrative linkage-spanning the years 1988-2014-to evaluate potential mediating pathways through socioeconomic status (SES), lifestyle, and health-related characteristics.

Results: Compared with Non-Hispanic White (NHW) adults, Non-White adults had a higher incidence of AD-specific (hazard ratio [HR] = 2.

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Background: Synucleinopathies are a group of neurodegenerative disorders that are pathologically characterized by intracellular aggregates called Lewy bodies. Lewy bodies are primarily composed of α-synuclein (asyn) protein, which is mostly phosphorylated at serine 129 (pS129) when aggregated and therefore used as a marker for pathology. Currently commercial antibodies against pS129 asyn stain aggregates well but in healthy brains cross react with other proteins, thus making it difficult to specifically detect physiological pS129 asyn.

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Differential racial and socioeconomic disparities in dementia incidence across income groups and their underlying mechanisms remain largely unknown. A retrospective cohort study examining all-cause dementia incidence across income groups was conducted linking third National Health and Nutrition Examination Surveys (NHANES III) to Centers for Medicare and Medicaid Services-Medicare data over ≤26 y of follow-up (1988-2014). Cox regression and generalized structural equations models (GSEM) were constructed among adults aged≥60 y at baseline (N = 4,592).

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Background: Although diets rich in carotenoids are associated with reduced risks of cardiovascular disease, age-related macular degeneration, disability, and other adverse aging outcomes, the underlying biological mechanisms are not fully elucidated.

Objectives: To characterize the plasma proteome fingerprint associated with circulating carotenoid and retinol concentrations in older adults.

Methods: In 728 adults ≥65 y participating in the Invecchiare in Chianti (InCHIANTI) Study, plasma α-carotene, β-carotene, β-cryptoxanthin, lutein, zeaxanthin, and lycopene were measured using HPLC.

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Mutant three-repeat tau expression initiates retinal ganglion cell death through Caspase-2.

Neurobiol Dis

May 2021

Department of Neurosciences, University of California, San Diego, School of Medicine, La Jolla, CA 92093, United States of America; Veterans Affairs San Diego Healthcare System, San Diego, CA 92161, United States of America. Electronic address:

The microtubule-associated protein tau is implicated in multiple degenerative diseases including retinal diseases such as glaucoma; however, the way tau initiates retinopathy is unclear. Previous retinal assessments in mouse models of tauopathy suggest that mutations in four-repeat (4R) tau are associated with disease-induced retinal dysfunction, while shifting tau isoform ratio to favor three-repeat (3R) tau production enhanced photoreceptor function. To further understand how alterations in tau expression impact the retina, we analyzed the retinas of transgenic mice overexpressing mutant 3R tau (m3R tau-Tg), a model known to exhibit Pick's Disease pathology in the brain.

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Introduction: Chronic kidney disease (CKD) is an important cause of disability and death, but its pathogenesis is poorly understood. Plasma metabolites can provide insights into underlying processes associated with CKD.

Objectives: To clarify the relationship of plasma metabolites with CKD and renal function in human.

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Co-infection between Helicobacter pylori (Hp) and groups of periodontal pathogens may alter the onset of Alzheimer's disease (AD) and all-cause dementia. We examined the interactive associations among Hp sero-positivity, periodontal disease (Pd), and infections with incident AD and all-cause dementia, among older adults (≥65 years at baseline). Up to 1431 participants from phase 1 of the National Health and Nutrition Survey III (1988-1991) had complete data till January 1st, 2014 on Hp sero-positivity with a mean follow-up of 10-11 years for AD and all-cause dementia incidence.

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Microbial agents including periodontal pathogens have recently appeared as important actors in Alzheimer's disease (AD) pathology. We examined associations of clinical periodontal and bacterial parameters with incident all-cause and AD dementia as well as AD mortality among US middle-aged and older adults. Clinical [Attachment Loss (AL); probing pocket depth (PPD)] and bacterial [pathogen immunoglobulin G (IgG)] periodontal markers were investigated in relation to AD and all-cause dementia incidence and to AD mortality, using data from the third National Health and Nutrition Examination Surveys (NHANES III, 1988-1994) linked longitudinally with National Death Index and Medicare data through January 1, 2014, with up to 26 years of follow-up.

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Dementia with Lewy bodies (DLB) is a clinically heterogeneous disorder with a substantial burden on healthcare. Despite this, the genetic basis of the disorder is not well defined and its boundaries with other neurodegenerative diseases are unclear. Here, we performed whole exome sequencing of a cohort of 1118 Caucasian DLB patients, and focused on genes causative of monogenic neurodegenerative diseases.

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p.V363I mutation: A rare cause of corticobasal degeneration.

Neurol Genet

August 2019

Neurodegenerative Disease Research Unit (S.A., M.S.S., S.W.S.), National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD; Movement Disorders and Memory Unit (M.D.F., P.P.), Department of Neurology, University Hospital Mutua de Terrassa, and Fundació per la Recerca Biomèdica i Social Mútua Terrassa, Barcelona, Spain; Laboratory of Neurogenetics (J.D.), National Institutes on Aging, National Institutes of Health, Bethesda, MD; Neurology Service (L.I.), Hospital Universitari Germans Trias, Pujol, Badalona, Spain; Department of Neurology (A.B., A.P., S.W.S.), Johns Hopkins University Medical Center, Baltimore, MD; Newcastle Institute for Ageing (C.M.M.), Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, United Kingdom; Department of Neurodegenerative Diseases (C.S., T.G.), Center of Neurology, Hertie-Institute for Clinical Brain Research, University of Tuebingen, and German Center for Neurodegenerative Diseases, Germany; Department of Molecular and Clinical Neuroscience (E.J., H.R.M.), Institute of Neurology, University College London, United Kingdom; Department of Pathology (Neuropathology) (O.P., J.T.), Johns Hopkins University Medical Center, Baltimore, MD; Department of Clinical Neurosciences (H.R.M.), Royal Free Campus UCL, Institute of Neurology, London, United Kingdom; Neurological Tissue Bank (E.G.), University of Barcelona-Hospital Clinic, IDIBAPS, Barcelona, Spain; and Institute of Neurology (E.G.), Medical University of Vienna, Austria.

Objective: Patients with corticobasal syndrome (CBS) present with heterogeneous clinical features, including asymmetric parkinsonism, dyspraxia, aphasia, and cognitive impairment; to better understand the genetic etiology of this rare disease, we undertook a genetic analysis of microtubule-associated protein tau ().

Methods: We performed a genetic evaluation of mutations in 826 neurologically healthy controls and 173 cases with CBS using the Illumina NeuroChip genotyping array.

Results: We identified 2 patients with CBS heterozygous for a rare mutation in (p.

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Mitochondrial oxidative stress accumulates with aging and age-related diseases and induces alterations in mitochondrial DNA (mtDNA) content. Since mtDNA qualitative alterations are also associated with aging, repair of mtDNA damage is of great importance. The most relevant form of DNA repair in this context is base excision repair (BER), which removes oxidized bases such as 8-oxoguanine (8-oxoG) and thymine glycol through the action of the mitochondrial isoform of the specific 8-oxoG DNA glycosylase/apurinic or apyrimidinic (AP) lyase (OGG1) or the endonuclease III homolog (NTH1).

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Author Correction: Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function.

Nat Commun

May 2019

Centre for Cognitive Ageing and Cognitive Epidemiology, Department of Psychology, School of Philosophy, Psychology and Language Sciences, The University of Edinburgh, Edinburgh, EH8 9JZ, UK.

Christina M. Lill, who contributed to analysis of data, was inadvertently omitted from the author list in the originally published version of this article. This has now been corrected in both the PDF and HTML versions of the article.

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C9orf72 hexanucleotide repeat length in older population: normal variation and effects on cognition.

Neurobiol Aging

December 2019

Molecular Neurology, Research Programs Unit, Department of Neurology, University of Helsinki, Helsinki University Hospital, Helsinki, Finland.

The hexanucleotide repeat expansion in C9orf72 is a common cause of amyotrophic lateral sclerosis/frontotemporal dementia and also rarely found in other psychiatric and neurodegenerative conditions. Alleles with >30 repeats are often considered an expansion, but the pathogenic repeat length threshold is still unclear. It is also unclear whether intermediate repeat length alleles (often defined either as 7-30 or 20-30 repeats) have clinically significant effects.

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Heritability and genetic variance of dementia with Lewy bodies.

Neurobiol Dis

July 2019

Department of Neurodegenerative Diseases, UCL Institute of Neurology, London, UK; UK Dementia Research Institute (UK DRI) at UCL, London, UK. Electronic address:

Article Synopsis
  • Recent genetic studies have revealed significant risk variants affecting dementia with Lewy bodies (DLB), showing that common variants explain a limited portion of its genetic basis.
  • The estimated heritability of DLB is significantly higher than past studies suggested, at 59.9%, indicating more complex genetic factors at play.
  • Genetic correlation analysis revealed DLB is positively associated with education levels, contrasting with the relationship found in Alzheimer's disease, suggesting the need for larger genome-wide association studies (GWAS) to uncover new genetic risk factors for DLB.
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A comprehensive screening of copy number variability in dementia with Lewy bodies.

Neurobiol Aging

March 2019

Department of Neurodegenerative Disease, UCL Institute of Neurology, London, UK; UK Dementia Research Institute (UK DRI) at UCL, London, UK; Department of Medical Sciences and Institute of Biomedicine, iBiMED, University of Aveiro, Aveiro, Portugal. Electronic address:

The role of genetic variability in dementia with Lewy bodies (DLB) is now indisputable; however, data regarding copy number variation (CNV) in this disease has been lacking. Here, we used whole-genome genotyping of 1454 DLB cases and 1525 controls to assess copy number variability. We used 2 algorithms to confidently detect CNVs, performed a case-control association analysis, screened for candidate CNVs previously associated with DLB-related diseases, and performed a candidate gene approach to fully explore the data.

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Background: Type 2 diabetes (T2D) is a major chronic condition requiring management through lifestyle changes and recommended health service visits. Mobile health (mHealth) is a promising tool to encourage self-management, but few studies have investigated the impact of mHealth on health care utilization.

Objective: The objective of this analysis was to determine the change in 2-year health service utilization and whether utilization explained a 1.

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Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function.

Nat Commun

May 2018

Centre for Cognitive Ageing and Cognitive Epidemiology, Department of Psychology, School of Philosophy, Psychology and Language Sciences, The University of Edinburgh, Edinburgh, EH8 9JZ, UK.

General cognitive function is a prominent and relatively stable human trait that is associated with many important life outcomes. We combine cognitive and genetic data from the CHARGE and COGENT consortia, and UK Biobank (total N = 300,486; age 16-102) and find 148 genome-wide significant independent loci (P < 5 × 10) associated with general cognitive function. Within the novel genetic loci are variants associated with neurodegenerative and neurodevelopmental disorders, physical and psychiatric illnesses, and brain structure.

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