John F. Ervin

ORCID: 0000-0002-4446-0231
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Dementia and Cognitive Impairment Research
  • Neurological Disease Mechanisms and Treatments
  • Parkinson's Disease Mechanisms and Treatments
  • Cerebrovascular and genetic disorders
  • Neurological diseases and metabolism
  • S100 Proteins and Annexins
  • Cholinesterase and Neurodegenerative Diseases
  • Neuroscience and Neuropharmacology Research
  • Bioinformatics and Genomic Networks
  • Amyotrophic Lateral Sclerosis Research
  • Stress Responses and Cortisol
  • Diabetes Treatment and Management
  • Retinal Diseases and Treatments
  • Heat shock proteins research
  • Health, Environment, Cognitive Aging
  • Retinal Imaging and Analysis
  • Gene expression and cancer classification
  • Glaucoma and retinal disorders
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Genetic Neurodegenerative Diseases
  • Genital Health and Disease
  • Vanadium and Halogenation Chemistry
  • Medication Adherence and Compliance
  • Nuclear Receptors and Signaling

Duke Medical Center
2007-2024

Duke University Hospital
2005-2023

Duke University
2005-2022

Thomas Jefferson University
2019

Rowan University
2019

Neurology, Inc
2007

VA Palo Alto Health Care System
2005

University of Mississippi Medical Center
2005

Jackson Memorial Hospital
2005

Medical University of South Carolina
2005

Michael A. Hauser R. Rand Allingham Tin Aung Carly J. van der Heide Kent D. Taylor and 88 more Jerome I. Rotter Shih‐Hsiu J. Wang Pieter W. M. Bonnemaijer Susan Williams Sadiq M. Abdullahi Khaled K. Abu‐Amero Michael G. Anderson Stephen Akafo Mahmoud B Alhassan Ifeoma N. Asimadu Radha Ayyagari Saydou Bakayoko Prisca Biangoup Nyamsi Donald W. Bowden William Bromley Donald L. Budenz Trevor Carmichael Pratap Challa Yii‐Der Ida Chen Chimdi M Chuka-Okosa Jessica N. Cooke Bailey Vital Paulino Costa Dianne A. Cruz Harvey Dubiner John F. Ervin Robert Feldman Miles J. Flamme‐Wiese Douglas Gaasterland Sarah J. Garnai Christopher A. Girkin Nouhoum Guirou Xiuqing Guo Jonathan L. Haines Christopher J. Hammond Leon W. Herndon Thomas J. Hoffmann Christine M. Hulette Abba Hydara Robert P. Igo Eric Jorgenson Joyce Kabwe Ngoy Janvier Kilangalanga Nkiru Kizor-Akaraiwe Rachel W. Kuchtey Hasnaa Lamari Zheng Li Jeffrey M. Liebmann Yutao Liu Ruth J. F. Loos Mônica Barbosa de Melo Sayoko E. Moroi Joseph Msosa Robert F. Mullins Girish N. Nadkarni Abdoulaye Napo Maggie Ng Hugo Freire Nunes Ebenezer Obeng-Nyarkoh Anthony Anya Okeke Suhanya Okeke Olusegun Olaniyi Olusola Olawoye Mariana Borges Oliveira L. Pasquale Rodolfo A. Perez-Grossmann Margaret A. Pericak‐Vance Xuejun Qin Michèle Ramsay Serge Resnikoff Julia E. Richards Rui Barroso Schimiti Kar Seng Sim William Eric Sponsel Paulo Vinícius Svidnicki Alberta A. H. J. Thiadens Nkechi Judith Uche Cornelia M. van Duijn José Paulo Cabral de Vasconcellos Janey L. Wiggs Linda M. Zangwill Neil Risch Dan Milea Adeyinka Ashaye Caroline C. W. Klaver Robert N. Weinreb Allison E. Ashley‐Koch John H. Fingert Chiea Chuen Khor

<h3>Importance</h3> Primary open-angle glaucoma presents with increased prevalence and a higher degree of clinical severity in populations African ancestry compared European or Asian ancestry. Despite this, individuals remain understudied genomic research for blinding disorders. <h3>Objectives</h3> To perform genome-wide association study (GWAS) evaluate potential mechanisms pathogenesis loci associated primary glaucoma. <h3>Design, Settings, Participants</h3> A 2-stage GWAS discovery data...

10.1001/jama.2019.16161 article EN JAMA 2019-11-05

The frontotemporal dementias (FTDs) are a heterogeneous group of neurodegenerative disorders that characterized clinically by dementia, personality changes, language impairment, and occasionally extrapyramidal movement disorders. Historically, the diagnosis classification FTDs has been fraught with difficulties, especially regard to establishing consensus on neuropathologic diagnosis. Recently, an international scientists participated in conference develop such criteria. They recommended...

10.1093/jnen/64.5.420 article EN Journal of Neuropathology & Experimental Neurology 2005-05-01

Abstract Objective: It is currently unknown whether cerebrospinal fluid (CSF) neurosteroid levels are related to brain in humans. CSF and dehydroepiandrosterone (DHEA) elevated patients with Alzheimer’s disease (AD), but it unclear DHEA correlated within the same subject cohort. We therefore determined pregnenolone AD (n = 25) cognitively intact control subjects 16) both temporal cortex. Design: were by gas chromatography/mass spectrometry preceded HPLC. Frozen cortex specimens provided...

10.1210/jc.2007-1229 article EN The Journal of Clinical Endocrinology & Metabolism 2008-05-14

Our hypothesis is that changes in gene and protein expression are crucial to the development of late-onset Alzheimer&rsquo;s disease. Previously we examined how DNA alleles control downstream RNA transcripts those relationships changed We have now proteins incorporated into networks two separate series evaluated our outputs different cell lines. pipeline included following steps: (i) predicting quantitative trait loci; (ii) determining differential expression; (iii) analysing transcript...

10.1093/brain/awy215 article EN cc-by-nc Brain 2018-07-25

The Bryan Alzheimer Disease Research Center obtains postmortem human brain tissue from patients with disease (AD) and cognitively normal control subjects for molecular genetic research programs. A growing body of suggests that variations in gene transcript levels may contribute to the onset progression disease. Identifying how regulation expression affect AD requires use high-quality mRNA banked brains. present study was conducted establish quality suitability available future studies. We...

10.1097/nen.0b013e31815c196a article EN Journal of Neuropathology & Experimental Neurology 2007-12-01

The molecular genetic basis that leads to Lewy Body (LB) pathology in 15–20% of Alzheimer disease cases (LBV/AD) was largely unknown. Alpha-synuclein (SNCA) and Leucine-rich repeat kinase2 (LRRK2) have been implicated the pathogenesis Parkinson's (PD), prototype LB spectrum disorders. We tested association SNCA variants with AD. then stratified analyses by LRRK2 genotype. also investigated expression regulation relation pathology. evaluated differences SNCA-mRNA LRRK2-mRNA levels as a...

10.1093/hmg/ddu196 article EN Human Molecular Genetics 2014-04-28

Abstract Tuberous sclerosis complex (TSC) is a neurodevelopmental disorder caused by mutations in the TSC1 and TSC2 genes autosomal dominantly inherited. These cause hyperactivation of mammalian Target Rapamycin (mTOR) pathway, leading to development nonmalignant masses involving various organ systems. Patients with TSC also experience neuropsychiatric symptoms collectively termed Sclerosis Complex Associated Neuropsychiatric Disorder (TAND). Due research advancements TSC, patients now live...

10.1186/s40478-022-01330-x article EN cc-by Acta Neuropathologica Communications 2022-03-03

We analyzed smooth muscle actin (SMA) immunoreactivity in brain blood vessels of 10 ApoE 4,4 Alzheimer disease (AD) patients and 3,3 AD matched for age, sex, duration dementia. also examined cognitively neuropathologically normal controls age sex. Vascular SMA the arachnoid, grey matter, white matter was quantified by image analysis. There less all when compared to (p < 0.001). In addition, arachnoidal had than 0.05). is decreased vascular density with matched, controls. The severity loss...

10.1093/jnen/63.7.735 article EN Journal of Neuropathology & Experimental Neurology 2004-07-01

Autopsy information on cardiovascular damage was investigated for pathologically confirmed Alzheimer disease (AD) patients (n=84) and non-AD control (n=60). The 51 relevant items were entered into a grade-of-membership model to describe vascular in AD. Five latent groups identified "I: early-onset AD," "II: controls, cancer," "III: extensive atherosclerosis," "IV: late-onset AD, male," "V: female." Expectedly, Groups IV V had elevated APOE epsilon 4 frequency. Unexpectedly, there limited...

10.1155/jbb.2005.189 article EN cc-by BioMed Research International 2005-01-01

Abstract Corpora amylacea (CA) and their murine analogs, periodic acid Schiff (PAS) granules, are age-related, carbohydrate-rich structures that serve as waste repositories for aggregated proteins, damaged cellular organelles, other debris. The structure, morphology, suspected functions of CA in the brain imply disease relevance. Despite this, link between age-related neurodegenerative diseases, particularly Alzheimer’s (AD), remains poorly defined. We performed a neuropathological analysis...

10.1186/s40478-022-01409-5 article EN cc-by Acta Neuropathologica Communications 2022-08-08

Tau aggregates are present in multiple neurodegenerative diseases known as "tauopathies," including Alzheimer's disease (AD), Pick's (PiD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). Such misfolded tau therefore potential sources for tauopathy biomarker discovery. Using the antibody screening approach targeting high-molecular-weight aggregates, we tested several antibodies a comprehensive set of site-specific phospho-tau (p-tau) phosphorylation sites showing...

10.1021/acschemneuro.2c00342 article EN ACS Chemical Neuroscience 2022-11-09
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