Jasmeer P. Chhatwal
A5088915384- Dementia and Cognitive Impairment Research
- Alzheimer's disease research and treatments
- Functional Brain Connectivity Studies
- Advanced Neuroimaging Techniques and Applications
- Bioinformatics and Genomic Networks
- Neurological Disease Mechanisms and Treatments
- Health, Environment, Cognitive Aging
- Neuroinflammation and Neurodegeneration Mechanisms
- Frailty in Older Adults
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Advanced MRI Techniques and Applications
- Health Systems, Economic Evaluations, Quality of Life
- Intracerebral and Subarachnoid Hemorrhage Research
- Down syndrome and intellectual disability research
- Memory and Neural Mechanisms
- Cancer-related cognitive impairment studies
- Neuroscience and Neuropharmacology Research
- Cholinesterase and Neurodegenerative Diseases
- Tryptophan and brain disorders
- Cerebrovascular and Carotid Artery Diseases
- Blood Pressure and Hypertension Studies
- Neural dynamics and brain function
- Chronic Disease Management Strategies
- EEG and Brain-Computer Interfaces
- Neurological Disorders and Treatments
Massachusetts General Hospital
2016-2025
Harvard University
2016-2025
Brigham and Women's Hospital
2016-2025
Asan Medical Center
2024
Dankook University
2024
Ulsan College
2024
University of Ulsan
2024
Marion General Hospital
2024
Athinoula A. Martinos Center for Biomedical Imaging
2014-2023
Alzheimer’s Disease Neuroimaging Initiative
2022-2023
Objective Detection of focal brain tau deposition during life could greatly facilitate accurate diagnosis Alzheimer disease (AD), staging and monitoring progression, development disease‐modifying therapies. Methods We acquired positron emission tomography (PET) using 18 F T807 (AV1451), amyloid‐β PET 11 C Pittsburgh compound B (PiB) in older clinically normal individuals, symptomatic patients with mild cognitive impairment or AD dementia. Results found abnormally high cortical binding...
Positron emission tomography (PET) imaging now allows in vivo visualization of both neuropathologic hallmarks Alzheimer disease (AD): amyloid-β (Aβ) plaques and tau neurofibrillary tangles. Observing their progressive accumulation the brains clinically normal older adults is critically important to understand pathophysiologic cascade leading AD inform choice outcome measures prevention trials.To assess associations among Aβ, tau, cognition, measured during different observation periods for 7...
Alzheimer's disease (AD) is characterized by two hallmark molecular pathologies: amyloid aβ1-42 and Tau neurofibrillary tangles. To date, studies of functional connectivity MRI (fcMRI) in individuals with preclinical AD have relied on associations vivo measures pathology. With the recent advent Tau-PET tracers it now possible to extend investigations fcMRI a sample cognitively normal elderly humans regional Tau. We modeled across four major cortical association networks [default-mode network...
<h3>Importance</h3> Mounting evidence suggests that sex differences exist in the pathologic trajectory of Alzheimer disease. Previous literature shows elevated levels cerebrospinal fluid tau women compared with men as a function apolipoprotein E (APOE) ε4 status and β-amyloid (Aβ). What remains unclear is association regional deposition clinically normal individuals. <h3>Objective</h3> To examine cross-sectional between Aβ measured positron emission tomography (PET). <h3>Design, Setting...
<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...
Objectives Amyloid‐beta (Aβ) and tau pathologies are commonly observed among clinically normal older individuals at postmortem can now be detected with in vivo neuroimaging. The association interaction of these proteinopathies prospective cognitive decline aging preclinical Alzheimer's disease (AD) remains to fully elucidated. Methods One hundred thirty‐seven (age = 76.3 ± 6.22 years) participating the Harvard Aging Brain Study underwent Aβ ( 11 C‐Pittsburgh compound B) 18 F‐flortaucipir)...
Abstract Introduction Our objective was to investigate the effect of sex on cognitive decline within context amyloid β (Aβ) burden and apolipoprotein E genotype. Methods We analyzed sex‐specific effects Aβ‐positron emission tomography, apolipoprotein, rates change Preclinical Alzheimer Cognitive Composite‐5 across three cohorts, such as Alzheimer's Disease Neuroimaging Initiative, Australian Imaging, Biomarker Lifestyle, Harvard Aging Brain Study (n = 755; clinical dementia rating 0; age...
Identifying asymptomatic individuals at high risk of impending cognitive decline because Alzheimer disease is crucial for successful prevention dementia. Vascular and β-amyloid (Aβ) pathology commonly co-occur in older adults are significant causes impairment.To determine whether vascular Aβ burden act additively or synergistically to promote clinically normal adults; and, secondarily, evaluate the unique influence on prospective beyond that used imaging biomarkers, including burden,...
We provide a comparative <i>in vivo</i> examination of the brain network-based distribution two hallmarks Alzheimer9s disease (AD) pathology in cognitively normal individuals: (1) <i>Tau</i>, detected with novel positron emission tomography (PET) tracer known as <sup>18</sup>F-AV-1451; and (2) amyloid-β, quantified <sup>11</sup>C-PiB PET. used high-resolution graph-based approach to investigate local-to-local local-to-distributed cortical associations between maps gray matter intensity. Our...
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...
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...
Both the acquisition and extinction of conditioned fear appear to require basolateral amygdala (BLA). Because these two forms learning have opposing effects on expression fear, we hypothesized that they may modulate GABAergic tone differentially within BLA. Previously, reported gene for GABA A receptor clustering protein gephyrin was significantly downregulated in BLA after (Ressler et al., 2002). Here demonstrate an analogous decrease levels, together with a surface receptors acquisition,...
To investigate default mode network (DMN) functional connectivity MRI (fcMRI) in a large cross-sectional cohort of subjects from families harboring pathogenic presenilin-1 (PSEN1), presenilin-2 (PSEN2), and amyloid precursor protein (APP) mutations participating the Dominantly Inherited Alzheimer Network.Eighty-three mutation carriers 37 asymptomatic noncarriers same underwent fMRI during resting state at 8 centers United States, Kingdom, Australia. Using group-independent component...
Abstract Introduction Sensitive detection of cognitive decline over the course preclinical Alzheimer's disease is critical as field moves toward secondary prevention trials. Methods We examined amyloid β (Aβ)‐related change in several variations Alzheimer composite (PACC) and each individual PACC component clinically normal (CN) older participants Harvard Aging Brain Study. then Disease Cooperative Study Prevention Instrument a replication cohort. Results Aβ+ CN individuals demonstrated...