Carol F. Lippa
A5089576120- Alzheimer's disease research and treatments
- Dementia and Cognitive Impairment Research
- Parkinson's Disease Mechanisms and Treatments
- Amyotrophic Lateral Sclerosis Research
- Cholinesterase and Neurodegenerative Diseases
- Neurological diseases and metabolism
- Ginkgo biloba and Cashew Applications
- Neuroscience and Neuropharmacology Research
- Prion Diseases and Protein Misfolding
- Diet and metabolism studies
- Neurological disorders and treatments
- Genetic Neurodegenerative Diseases
- Health Systems, Economic Evaluations, Quality of Life
- Cerebrovascular and genetic disorders
- Neurogenetic and Muscular Disorders Research
- Nuclear Receptors and Signaling
- Neurobiology of Language and Bilingualism
- Epilepsy research and treatment
- Cellular transport and secretion
- Neurological and metabolic disorders
- S100 Proteins and Annexins
- Neuroinflammation and Neurodegeneration Mechanisms
- Health and Well-being Studies
- RNA regulation and disease
- Computational Drug Discovery Methods
University of Pennsylvania
2001-2024
Thomas Jefferson University Hospital
2018-2024
Thomas Jefferson University
2017-2024
University of Miami
2024
University of California, San Diego
2024
Cleveland Clinic
2023
Lou Ruvo Brain Institute
2023
Drexel University
2009-2019
Brigham and Women's Hospital
2015
University of Michigan–Ann Arbor
2015
A working group supported by the Office of Rare Diseases National Institutes Health formulated neuropathologic criteria for corticobasal degeneration (CBD) that were subsequently validated an independent neuropathologists. The do not require a specific clinical phenotype, since CBD can have diverse presentations, such as progressive asymmetrical rigidity and apraxia, aphasia, or frontal lobe dementia. Cortical atrophy, ballooned neurons, substantia nigra been emphasized in previous...
Missense mutations in the alpha-synuclein gene cause familial Parkinson's disease (PD), and is a major component of Lewy bodies (LBs) sporadic PD, dementia with LBs (DLB), LB variant Alzheimer's (AD). To determine whether AD (FAD) patients known presenilin (n = 65) or amyloid precursor protein 9) genes, studies were conducted antibodies to alpha-, beta-, gamma-synuclein. detected alpha- but not beta- gamma-synuclein 22% FAD brains, alpha-synuclein-positive most numerous amygdala where some...
The TAR DNA-binding protein 43 (TDP-43) has been identified as the major disease in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitin inclusions (FTLD-U), defining a novel class of neurodegenerative conditions: TDP-43 proteinopathies. first pathogenic mutations gene encoding (TARDBP) were recently reported familial sporadic ALS patients, supporting direct role for neurodegeneration. In this study, we report identification functional analyses two one...
The amyloid cascade hypothesis suggests that the aggregation and deposition of amyloid-β protein is an initiating event in Alzheimer9s disease (AD). Using imaging technology, such as positron emission tomography (PET) agent Pittsburgh compound-B (PiB), it possible to explore natural history preclinical people at high risk for AD. With this goal mind, asymptomatic (<i>n</i> = 5) symptomatic carriers presenilin-1 (PS1) mutations (C410Y or A426P) lead early-onset AD noncarrier controls from...
Abstract Background A rare variant in the Triggering Receptor Expressed on Myeloid cells 2 ( TREM2 ) gene has been reported to be a genetic risk factor for Alzheimer’s disease by two independent groups (Odds ratio between 2.9-4.5). Given key role of effective phagocytosis apoptotic neuronal microglia, we hypothesized that dysfunction may play more generalized neurodegeneration. With this mind set out assess association disease-related (rs75932628, p.R47H) with other related neurodegenerative...
Rare mutations in the gene encoding for tau (MAPT, microtubule-associated protein tau) cause frontotemporal dementia-spectrum (FTD-s) disorders, including FTD, progressive supranuclear palsy (PSP) and corticobasal syndrome, a common extended haplotype spanning across MAPT locus is associated with increased risk of PSP Parkinson's disease.We identified rare variant (p.A152T) patient clinical diagnosis assessed its frequency multiple independent series patients neurodegenerative conditions...
Immunohistochemical examination of 20 Down's syndrome brains, using antibodies to α-, β-, and γ-synuclein, demonstrated many α-synuclein–positive Lewy bodies dystrophic neurites in 50% amygdala samples from brains with Alzheimer's disease. Similar lesions were less common other regions these none which contained β-synuclein or γ-synuclein abnormalities. Thus, neuritic processes frequently occur disease brains. Ann Neurol 1999;45:353–357
<h3>Objectives:</h3> To determine whether <i>TMEM106B</i> single nucleotide polymorphisms (SNPs) are associated with frontotemporal lobar degeneration (FTLD) in patients and without mutations progranulin (<i>GRN</i>) to modulates <i>GRN</i> expression. <h3>Methods:</h3> We performed a case-control study of 3 SNPs 482 clinical 80 pathologic FTLD–TAR DNA-binding protein 43 mutations, 78 FTLD 822 controls. Association analysis GRN plasma levels was 1,013 controls mRNA expression were correlated...
Expanded glutamine repeats of the ataxin-2 (ATXN2) protein cause spinocerebellar ataxia type 2 (SCA2), a rare neurodegenerative disorder. More recent studies have suggested that expanded ATXN2 are genetic risk factor for amyotrophic lateral sclerosis (ALS) via an RNA-dependent interaction with TDP-43. Given phenotypic diversity observed in SCA2 patients, we set out to determine polymorphic nature repeat length across spectrum disorders. In this study, genotyped 3919 disease patients and 4877...
Background: Clinical trials of anti-Aβ monoclonal antibodies in Alzheimer disease (AD) infer target engagement from Aβ positron emission tomography (PET) and/or fluid biomarkers such as cerebrospinal (CSF) Aβ42/40.However, these measure deposits indirectly incompletely.In contrast, postmortem neuropathologic assessments allow direct investigation treatment effects on brain and many other pathologic features.Methods: From a clinical trial dominantly inherited AD, we measured...
We compared immunohistochemical expression of the transforming growth factor-betas (TGF-beta 1, TGF-beta 2, and 3) using brain tissue from patients with nondominantly inherited Alzheimer's disease (NDAD) (n = 9), autosomal dominantly linkage to 14q24.3 (FAD-14) 4), cognitively normal controls 10) determine whether their pathologic changes are associated an altered distribution TGF-betas. found increased 2 in large, tangle-bearing neurons widespread staining glia NDAD FAD-14 control cases....