Sarah Berman
A5023066705- Dementia and Cognitive Impairment Research
- Alzheimer's disease research and treatments
- Parkinson's Disease Mechanisms and Treatments
- Functional Brain Connectivity Studies
- Mitochondrial Function and Pathology
- Bioinformatics and Genomic Networks
- Advanced Neuroimaging Techniques and Applications
- Frailty in Older Adults
- Genetic Neurodegenerative Diseases
- Down syndrome and intellectual disability research
- Neuroscience and Neuropharmacology Research
- Health, Environment, Cognitive Aging
- Autophagy in Disease and Therapy
- Health Systems, Economic Evaluations, Quality of Life
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological disorders and treatments
- Chronic Disease Management Strategies
- Genetic Associations and Epidemiology
- Statistical Methods in Clinical Trials
- Neurological diseases and metabolism
- Neurological Disease Mechanisms and Treatments
- Metabolism and Genetic Disorders
- Tryptophan and brain disorders
- Amyloidosis: Diagnosis, Treatment, Outcomes
- S100 Proteins and Annexins
University of Pittsburgh
2015-2025
University of Pittsburgh Medical Center
2021-2025
Institute for Neurodegenerative Disorders
2010-2024
Thomas Jefferson University
2024
University of Miami
2024
University of California, San Diego
2024
University of Pennsylvania
2024
University of Ulsan
2024
Asan Medical Center
2024
Dankook University
2024
Abstract : Both reactive dopamine metabolites and mitochondrial dysfunction have been implicated in the neurodegeneration of Parkinson’s disease. Dopamine metabolites, quinone oxygen species, can directly alter protein function by oxidative modifications, several proteins may be targets this damage. In study, we examined, using isolated brain mitochondria, whether oxidation products function. We found that exposure to caused a large increase resting state 4 respiration. This effect was...
<h3>Objective</h3> To assess the onset, sequence, and rate of progression comprehensive biomarker clinical measures across spectrum Alzheimer disease (AD) using Dominantly Inherited Network (DIAN) study compare these to cross-sectional estimates. <h3>Methods</h3> We conducted longitudinal clinical, cognitive, CSF, neuroimaging assessments (mean 2.7 [±1.1] visits) in 217 DIAN participants. Linear mixed effects models were used changes each measure relative individuals9 estimated years symptom...
Macrophages are important players in the maintenance of tissue homeostasis1. Perivascular and leptomeningeal macrophages reside near central nervous system (CNS) parenchyma2, their role CNS physiology has not been sufficiently well studied. Given continuous interaction with cerebrospinal fluid (CSF) strategic positioning, we refer to these cells collectively as parenchymal border (PBMs). Here demonstrate that PBMs regulate CSF flow dynamics. We identify a subpopulation express high levels...
Tauopathy is a hallmark pathology of Alzheimer's disease with strong relationship cognitive impairment. As such, understanding tau may be key to clinical interventions. In vivo tauopathy has been measured using cerebrospinal fluid assays, but these do not provide information about where in the brain. The introduction PET ligands that bind paired helical filaments provides ability measure amount and distribution pathology. heritability age dementia onset tied specific mutations found...
Therapeutic modulation of TREM2-dependent microglial function might provide an additional strategy to slow the progression Alzheimer's disease. Although studies in animal models suggest that TREM2 is protective against pathology, its effect on tau pathology and potential beneficial role people with disease still unclear. Our aim was study associations between dynamics soluble TREM2, as a biomarker signalling, amyloid β (Aβ) deposition, tau-related neuroimaging markers, cognitive decline,...
Abstract Alzheimer’s disease (AD) pathology develops many years before the onset of cognitive symptoms. Two pathological processes—aggregation amyloid-β (Aβ) peptide into plaques and microtubule protein tau neurofibrillary tangles (NFTs)—are hallmarks disease. However, other brain processes are thought to be key mediators Aβ plaque NFT pathology. How these additional pathologies evolve over course is currently unknown. Here we show that proteomic measurements in autosomal dominant AD...
Abstract We present a comprehensive global analysis of genetic variants associated with autosomal-dominant Alzheimer's disease (ADAD). A total 550 in the APP, PSEN1, and PSEN2 genes were identified, which 279 classified as pathogenic or likely based on ACMG-AMP criteria, utilizing data from Dominantly Inherited Alzheimer Network (DIAN), literature, public databases. Symptomatic age at onset (AAO) was estimated for 227 these variants, allowing detailed characterization their frequency,...
Mitochondrial fission and fusion are linked to synaptic activity in healthy neurons implicated the regulation of apoptotic cell death many types. We developed fluorescence microscopy computational strategies directly measure mitochondrial frequencies their effects on morphology cultured neurons. found that rate exceeds neuronal processes, and, therefore, fission/fusion ratio alone is insufficient explain at steady state. This imbalance between compensated by growth organelles. Bcl-xL...
Recent studies delineate a pathway involving familial Parkinson's disease (PD)-related proteins PINK1 and Parkin, in which PINK1-dependent mitochondrial accumulation of Parkin targets depolarized mitochondria towards degradation through mitophagy. The has been primarily characterized cells less dependent on for energy production than neurons. Here we report that neurons, unlike other cells, depolarization by carbonyl cyanide m-chlorophenyl hydrazone did not induce translocation to or...
Abstract: Dopamine can oxidize to form reactive oxygen species and quinones, we have previously shown that dopamine quinones bind covalently cysteinyl residues on striatal proteins. The transporter is one of the proteins at risk for this modification, because it has a high affinity contains several residues. Therefore, tested whether transport in rat synaptosomes could be affected by generators species, including dopamine. Uptake [ 3 H]dopamine (250 n M ) was inhibited ascorbate (0.85 m ;...
Quantitative in vivo measurement of brain amyloid burden is important for both research and clinical purposes. However, the existence multiple imaging tracers presents challenges to interpretation such measurements. This study a direct comparison Pittsburgh compound B-based florbetapir-based same participants from two independent cohorts using crossover design.Pittsburgh B florbetapir PET data three different were analyzed previously established pipelines obtain global These measurements...
Abstract Cognitive resilience is an important modulating factor of cognitive decline in Alzheimer’s disease, but the functional brain mechanisms that support remain elusive. Given previous findings normal ageing, we tested hypothesis higher segregation brain’s connectome into distinct networks represents a mechanism underlying disease. Using resting-state MRI, assessed both MRI global system segregation, i.e. balance between-network to within-network connectivity, and alternate index...
"Brain-predicted age" quantifies apparent brain age compared to normative neuroimaging trajectories. Advanced brain-predicted has been well established in symptomatic Alzheimer disease (AD), but is underexplored preclinical AD. Prior studies have typically used structural MRI, resting-state functional connectivity (FC) remains underexplored. Our model predicted from FC 391 cognitively normal, amyloid-negative controls (ages 18-89). We applied the trained 145 amyloid-negative, 151 AD, and 156...