James B. Leverenz
A5052130722- Alzheimer's disease research and treatments
- Dementia and Cognitive Impairment Research
- Parkinson's Disease Mechanisms and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological Disease Mechanisms and Treatments
- Neurological disorders and treatments
- Ginkgo biloba and Cashew Applications
- Cholinesterase and Neurodegenerative Diseases
- Neurological diseases and metabolism
- Nuclear Receptors and Signaling
- Bioinformatics and Genomic Networks
- Neuroscience and Neuropharmacology Research
- Inflammation biomarkers and pathways
- Amyotrophic Lateral Sclerosis Research
- Genetic Associations and Epidemiology
- Health, Environment, Cognitive Aging
- Folate and B Vitamins Research
- Advanced Neuroimaging Techniques and Applications
- Medical Imaging Techniques and Applications
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Functional Brain Connectivity Studies
- Genetic Neurodegenerative Diseases
- Computational Drug Discovery Methods
- Tryptophan and brain disorders
- Long-Term Effects of COVID-19
Cleveland Clinic
2016-2025
Lou Ruvo Brain Institute
2015-2024
Cleveland Clinic Lerner College of Medicine
2021-2024
University of Iowa
2024
Rutgers, The State University of New Jersey
2024
University of Pennsylvania
2012-2024
University of California, San Diego
2008-2024
University of Miami
2015-2024
Thomas Jefferson University
2024
McMaster Children's Hospital
2024
Disorders of the brain can exhibit considerable epidemiological comorbidity and often share symptoms, provoking debate about their etiologic overlap. We quantified genetic sharing 25 disorders from genome-wide association studies 265,218 patients 784,643 control participants assessed relationship to 17 phenotypes 1,191,588 individuals. Psychiatric common variant risk, whereas neurological appear more distinct one another psychiatric disorders. also identified significant between a number...
Variants in triggering receptor expressed on myeloid cells 2 (TREM2) confer high risk for Alzheimer’s disease (AD) and other neurodegenerative diseases. However, the cell types mechanisms underlying TREM2’s involvement neurodegeneration remain to be established. Here, we report that TREM2 is up-regulated surrounding amyloid deposits AD mouse models human tissue. was detected CD45hiLy6C+ cells, but not P2RY12+ parenchymal microglia. In mice deficient TREM2, macrophages are virtually...
Biomarkers are urgently needed for the diagnosis and monitoring of disease progression in Parkinson’s disease. Both DJ-1 α-synuclein, two proteins critically involved pathogenesis, have been tested as biomarkers several recent studies with inconsistent results. These largely due to variation protein species detected by different antibodies, limited numbers patients some studies, or inadequate control important variables. In this study, nature α-synuclein human cerebrospinal fluid was studied...
Abstract Background Evaluation of brain β‐amyloid by positron emission tomography (PET) imaging can assist in the diagnosis Alzheimer disease (AD) and other dementias. Methods Open‐label, nonrandomized, multicenter, phase 3 study to validate 18 F‐labeled tracer florbetaben comparing vivo PET with post‐mortem histopathology. Results Brain images tissue from 74 deceased subjects (of 216 trial participants) were analyzed. Forty‐six 47 neuritic β‐amyloid‐positive cases read as positive, 24 27...
Abstract Objective: A study was undertaken to examine the neuropathological substrates of cognitive dysfunction and dementia in Parkinson disease (PD). Methods: One hundred forty patients with a clinical diagnosis PD either normal cognition or onset 2 more years after motor symptoms (PDD) were studied. Patients Lewy bodies excluded. Autopsy records genetic data semiquantitative scores for burden neurofibrillary tangles, senile plaques, (LBs), neurites (LNs) other pathologies used develop...
Abstract Objective Previously published community‐ or population‐based studies of brain aging and dementia with autopsy were restricted to a single sex, ethnic group, Roman Catholic clergy, focused pathological assessments. Our goal was determine the independent correlates associated in typical US population. Methods We evaluated data from Adult Changes Thought study, an ongoing longitudinal, study dementia. Analyses based on collected about 3,400 people 65 years older who cognitively intact...
OBJECTIVES : Most clinico‐neuropathological correlative studies of Alzheimer's Disease (AD) are based on research cohorts that not necessarily generalizable to patients seen in the general medical community. In this study, we examine accuracy criteria used diagnosing AD a community‐based case series with memory complaints. DESIGN AND PARTICIPANTS Clinical and neuropathological diagnoses were obtained from 134 evaluated for dementia who subsequently underwent autopsy. SETTING Subjects...
Abstract Objective: There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring progression. We others have demonstrated that decrease in DJ‐1 and/or α‐synuclein the cerebrospinal fluid (CSF) potential index but not PD severity. Methods: Using highly sensitive quantitative Luminex assays, we measured total tau, phosphorylated amyloid beta peptide 1–42 (Aβ ), Flt3 ligand, fractalkine levels CSF large cohort...
The late effects of traumatic brain injury (TBI) are great interest, but studies characterizing these limited.
Biomarkers are needed to assist in the diagnosis and medical management of various neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's (PD), dementia with Lewy body (DLB). We have employed a multiplex quantitative
PAR promotes α-synuclein toxicity How pathologic (α-syn) leads to neurodegeneration in Parkinson's disease (PD) remains poorly understood. Kam et al. studied the α-syn preformed fibril (α-syn PFF) model of sporadic PD (see Perspective by Brundin and Wyse). They found that α-syn–activated poly(adenosine 5′-diphosphate–ribose) (PAR) polymerase–1 (PARP-1) inhibition PARP or knockout PARP-1 protected mice from pathology. The generation PFF–induced activation converted PFF a strain was 25-fold...
<h3>Importance</h3> We observed a significant correlation between cerebrospinal fluid (CSF) levels of tau proteins and α-synuclein, but not β-amyloid 1-42 (Aβ1-42), lower concentration CSF biomarkers, as compared with healthy controls, in cohort entirely untreated patients Parkinson disease (PD) at the earliest stage studied so far. <h3>Objective</h3> To evaluate baseline characteristics relationship to clinical features biomarkers (Aβ1-42, total [T-tau], phosphorylated threonine 181...
<h3>Objective</h3>To test for an association between the apolipoprotein E (APOE) ϵ4 allele and dementias with synucleinopathy.<h3>Design</h3>Genetic case-control study.<h3>Setting</h3>Academic research.<h3>Patients</h3>Autopsied subjects were classified into 5 categories: dementia high-level Alzheimer disease (AD) neuropathologic changes (NCs) but without Lewy body (LBD) NCs (AD group; n = 244), LBDNCs ADNCs (LBD-AD 224), no or low levels of (pure DLB [pDLB] 91), Parkinson (PDD) (n 81),...
Abstract This study was undertaken to determine the prevalence and correlates of cognitive impairment (CI) neuropsychiatric symptoms (NPS) in early, untreated patients with Parkinson's disease (PD). Background Both CI NPS are common PD impact course quality life. However, limited knowledge is available about abilities NPS. Methods Progression Markers Initiative (PPMI) a multi‐site healthy controls (HCs), latter normal cognition. At baseline, participants were assessed neuropsychological...