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Alzheimer Disease: HELP
Articles by Jared R. Brosch
Based on 6 articles published since 2010
(Why 6 articles?)
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Between 2010 and 2020, Jared R. Brosch wrote the following 6 articles about Alzheimer Disease.
 
+ Citations + Abstracts
1 Review Tau Imaging in Alzheimer's Disease Diagnosis and Clinical Trials. 2017

Brosch, Jared R / Farlow, Martin R / Risacher, Shannon L / Apostolova, Liana G. ·Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, USA. jbrosch@iu.edu. · Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, USA. · Department of Radiological Sciences, Indiana University School of Medicine, Indianapolis, IN, USA. · Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA. ·Neurotherapeutics · Pubmed #27873182.

ABSTRACT: In vivo imaging of the tau protein has the potential to aid in quantitative diagnosis of Alzheimer's disease, corroborate or dispute the amyloid hypothesis, and demonstrate biomarker engagement in clinical drug trials. A host of tau positron emission tomography agents have been designed, validated, and tested in humans. Several agents have characteristics approaching the ideal imaging tracer with some limitations, primarily regarding off-target binding. Dozens of clinical trials evaluating imaging techniques and several pharmaceutical trials have begun to integrate tau imaging into their protocols.

2 Review Immunotherapy for Alzheimer's disease. 2013

Farlow, Martin R / Brosch, Jared R. ·Department of Neurology, Indiana University School of Medicine, 355 West 16th Street, Suite 4700, Indianapolis, IN 46202, USA. mfarlow@iupui.edu ·Neurol Clin · Pubmed #23896510.

ABSTRACT: The immune system plays a significant role in Alzheimer disease (AD). β-Amyloid deposition in the cortex is thought to be an initiating event in AD and the widely believed amyloid hypothesis proposes removal of amyloid may delay disease progression. Human trials of active or passive immune agents have failed to show benefit and increased adverse events of vasogenic edema and microhemorrhages. Evidence suggests the illness may be too advanced by the time patients are symptomatic with dementia. Future directions include better understanding of how and where immunotherapies should be targeted and treating patients at earlier stages of the illness.

3 Article Visual contrast sensitivity is associated with the presence of cerebral amyloid and tau deposition. 2020

Risacher, Shannon L / WuDunn, Darrell / Tallman, Eileen F / West, John D / Gao, Sujuan / Farlow, Martin R / Brosch, Jared R / Apostolova, Liana G / Saykin, Andrew J. ·Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN, USA. · Indiana Alzheimer Disease Center, Indiana University School of Medicine, Indianapolis, IN, USA. · Department of Ophthalmology, UF College of Medicine-Jacksonville, Jacksonville, FL, USA. · Department of Biostatistics, Indiana University School of Medicine, Indianapolis, IN, USA. · Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, USA. ·Brain Commun · Pubmed #32309804.

ABSTRACT: Visual deficits are common in neurodegenerative diseases including Alzheimer's disease. We sought to determine the association between visual contrast sensitivity and neuroimaging measures of Alzheimer's disease-related pathophysiology, including cerebral amyloid and tau deposition and neurodegeneration. A total of 74 participants (7 Alzheimer's disease, 16 mild cognitive impairment, 20 subjective cognitive decline, 31 cognitively normal older adults) underwent the frequency doubling technology 24-2 examination, a structural MRI scan and amyloid PET imaging for the assessment of visual contrast sensitivity. Of these participants, 46 participants (2 Alzheimer's disease, 9 mild cognitive impairment, 12 subjective cognitive decline, 23 cognitively normal older adults) also underwent tau PET imaging with [

4 Article Tau PET in autosomal dominant Alzheimer's disease: relationship with cognition, dementia and other biomarkers. 2019

Gordon, Brian A / Blazey, Tyler M / Christensen, Jon / Dincer, Aylin / Flores, Shaney / Keefe, Sarah / Chen, Charles / Su, Yi / McDade, Eric M / Wang, Guoqiao / Li, Yan / Hassenstab, Jason / Aschenbrenner, Andrew / Hornbeck, Russ / Jack, Clifford R / Ances, Beau M / Berman, Sarah B / Brosch, Jared R / Galasko, Douglas / Gauthier, Serge / Lah, James J / Masellis, Mario / van Dyck, Christopher H / Mintun, Mark A / Klein, Gregory / Ristic, Smiljana / Cairns, Nigel J / Marcus, Daniel S / Xiong, Chengjie / Holtzman, David M / Raichle, Marcus E / Morris, John C / Bateman, Randall J / Benzinger, Tammie L S. ·Mallinckrodt Institute of Radiology, Washington University in St. Louis, MO, USA. · Knight Alzheimer's Disease Research Center, Washington University in St. Louis MO, USA. · The Hope Center for Neurological Disorders, St. Louis, MO, USA. · Department of Psychological and Brain Sciences, Washington University in St. Louis MO, USA. · Banner Health, Phoenix AZ, USA. · Department of Neurology, Washington University in St. Louis MO, USA. · Department of Radiology, Mayo Clinic, Rochester, MN, USA. · Department of Neurology, University of Pittsburgh, Pittsburgh, PA, USA. · Department of Neurology, Indiana University, Indianapolis, IN, USA. · Department of Neurosciences, University of California, San Diego, CA, USA. · Departments of Psychiatry, Neurology and Neurosurgery, and Medicine, McGill University, Montreal, Canada. · Department of Neurology, Emory University, Atlanta, GA, USA. · Division of Neurology, Sunnybrook Health Sciences Centre; Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute; Department of Medicine, University of Toronto, Toronto, ON, Canada. · Alzheimer's Disease Research Unit, Yale University School of Medicine, New Haven, CT, USA. · Avid Radiopharmaceuticals (A Wholly Owned Subsidiary of Eli Lilly and Company), Philadelphia, PA, USA. · Roche Pharma Research and Early Development, Basel, Switzerland. · Roche/Genentech Product Development, Neuroscience, Basel, Switzerland. · Department of Biostatistics, Washington University in St. Louis, MO, USA. ·Brain · Pubmed #30753379.

ABSTRACT: Tauopathy is a hallmark pathology of Alzheimer's disease with a strong relationship with cognitive impairment. As such, understanding tau may be a key to clinical interventions. In vivo tauopathy has been measured using cerebrospinal fluid assays, but these do not provide information about where pathology is in the brain. The introduction of PET ligands that bind to paired helical filaments provides the ability to measure the amount and distribution of tau pathology. The heritability of the age of dementia onset tied to the specific mutations found in autosomal dominant Alzheimer's disease families provides an elegant model to study the spread of tau across the course of the disease as well as the cross-modal relationship between tau and other biomarkers. To better understand the pathobiology of Alzheimer's disease we measured levels of tau PET binding in individuals with dominantly inherited Alzheimer's disease using data from the Dominantly Inherited Alzheimer Network (DIAN). We examined cross-sectional measures of amyloid-β, tau, glucose metabolism, and grey matter degeneration in 15 cognitively normal mutation non-carriers, 20 asymptomatic carriers, and 15 symptomatic mutation carriers. Linear models examined the association of pathology with group, estimated years to symptom onset, as well as cross-modal relationships. For comparison, tau PET was acquired on 17 older adults with sporadic, late onset Alzheimer disease. Tau PET binding was starkly elevated in symptomatic DIAN individuals throughout the cortex. The brain areas demonstrating elevated tau PET binding overlapped with those seen in sporadic Alzheimer's disease, but with a greater cortical involvement and greater levels of binding despite similar cognitive impairment. Tau PET binding was elevated in the temporal lobe, but the most prominent loci of pathology were in the precuneus and lateral parietal regions. Symptomatic mutation carriers also demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-β. The degree of tau tracer binding in symptomatic individuals was correlated to other biomarkers, particularly markers of neurodegeneration. In addition to the differences seen with tau, amyloid-β was increased in both asymptomatic and symptomatic groups relative to non-carriers. Glucose metabolism showed decline primarily in the symptomatic group. MRI indicated structural degeneration in both asymptomatic and symptomatic cohorts. We demonstrate that tau PET binding is elevated in symptomatic individuals with dominantly inherited Alzheimer's disease. Tau PET uptake was tied to the onset of cognitive dysfunction, and there was a higher amount, and different regional pattern of binding compared to late onset, non-familial Alzheimer's disease.

5 Article Patient and Caregiver Assessment of the Benefits From the Clinical Use of Amyloid PET Imaging. 2018

Mustafa, Rafid / Brosch, Jared R / Rabinovici, Gil D / Dickerson, Bradford C / Carrillo, Maria C / Glazier, Bradley S / Gao, Sujuan / Tierney, Martha / Fargo, Keith N / Austrom, Mary G / De Santi, Susan / Clark, David G / Apostolova, Liana G. ·Indiana University School of Medicine. · Departments of Neurology. · Department of Neurology, University of California San Francisco, San Francisco, CA. · Department of Neurology, Harvard Medical School and Massachusetts General Hospital. · Division of Medical & Scientific Relations, Alzheimer's Association, Chicago, IL. · Radiology. · Biostatistics. · Psychiatry. · Piramal Pharma Inc, Boston, MA. · Department of Neurology, Medical University of South Carolina. · Department of Neurology, Ralph H. Johnson VA Medical Center, Charleston, SC. · Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN. ·Alzheimer Dis Assoc Disord · Pubmed #29140859.

ABSTRACT: INTRODUCTION: Few studies to date have explored patient and caregiver views on the clinical use of amyloid positron emission tomography (PET). METHODS: A 7-item questionnaire assessing patient and caregiver views (510 total respondents) toward amyloid PET imaging was advertised broadly through alz.org/trialmatch. RESULTS: We received 510 unique responses from 48 US states, 2 Canadian provinces, the Dominican Republic, and Greece. Both patients and caregivers indicated that they would want to receive amyloid imaging if offered the opportunity. Over 88% of respondents had a positive response (∼10% with neutral and 2% with negative responses) to whether amyloid PET should be offered routinely and be reimbursed. Such information was felt to be useful for long-term legal, financial, and health care planning. Respondents identifying with early age cognitive decline (younger than 65 y) were more likely to explore options for disability insurance (P=0.03). Responders from the Midwest were more likely to utilize information from amyloid imaging for legal planning (P=0.02), disability insurance (P=0.02), and life insurance (P=0.04) than other US regions. DISCUSSION: Patients and caregivers supported the use of amyloid PET imaging in clinical practice and felt that the information would provide significant benefits particularly in terms of future planning.

6 Article Journal Club: comparison of symptomatic and asymptomatic persons with Alzheimer disease neuropathology. 2014

Brosch, Jared R / Matthews, Brandy R. ·From the Department of Neurology, Indiana University School of Medicine, Indianapolis. ·Neurology · Pubmed #24590252.

ABSTRACT: -- No abstract --