D
David G. Coughlin
Researcher at University of Pennsylvania
Publications - 36
Citations - 707
David G. Coughlin is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Medicine & Progressive supranuclear palsy. The author has an hindex of 10, co-authored 21 publications receiving 344 citations. Previous affiliations of David G. Coughlin include Pennsylvania Hospital & University of California, San Diego.
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Journal ArticleDOI
Distribution patterns of tau pathology in progressive supranuclear palsy
Gabor G. Kovacs,Gabor G. Kovacs,Gabor G. Kovacs,Milica Ječmenica Lukić,Milica Ječmenica Lukić,David J. Irwin,Thomas Arzberger,Gesine Respondek,Gesine Respondek,Gesine Respondek,Edward B. Lee,David G. Coughlin,David G. Coughlin,Armin Giese,Murray Grossman,Carolin Kurz,Carolin Kurz,Corey T. McMillan,Ellen Gelpi,Ellen Gelpi,Yaroslau Compta,John C. van Swieten,Laura Donker Laat,Claire Troakes,Safa Al-Sarraj,John L. Robinson,Sigrun Roeber,Sharon X. Xie,Virginia M.-Y. Lee,John Q. Trojanowski,Günter U. Höglinger +30 more
TL;DR: Defining cell-specific stages of tau pathology helps to identify preclinical or early-stage cases for the better understanding of early pathogenic events, has implications for understanding the clinical subtype-specific dynamics of disease-propagation, and informs tau-neuroimaging on distribution patterns.
Journal ArticleDOI
Cognitive and Pathological Influences of Tau Pathology in Lewy Body Disorders
David G. Coughlin,Sharon X. Xie,Mendy Liang,Andrew Williams,Claire Peterson,Daniel Weintraub,Daniel Weintraub,Corey T. McMillan,David A. Wolk,Rizwan S. Akhtar,Howard I. Hurtig,H. Branch Coslett,Roy H. Hamilton,Andrew Siderowf,John E. Duda,John E. Duda,Katya Rascovsky,Edward B. Lee,Virginia M.-Y. Lee,Murray Grossman,John Q. Trojanowski,David J. Irwin +21 more
TL;DR: Using digital histology in a large autopsy cohort of Lewy body disorder patients with dementia to test the hypotheses that co‐occurring Alzheimer disease pathology impacts the anatomic distribution of α‐synuclein (SYN) pathology and that co-occurring neocortical tau pathology in LBDs associates with worse cognitive performance and occurs in a pattern differing from AD.
Journal ArticleDOI
CSF tau and β-amyloid predict cerebral synucleinopathy in autopsied Lewy body disorders.
David J. Irwin,Sharon X. Xie,David G. Coughlin,Naomi Nevler,Rizwan S. Akhtar,Corey T. McMillan,Edward B. Lee,David A. Wolk,Daniel Weintraub,Alice Chen-Plotkin,John E. Duda,Meredith Spindler,Andrew Siderowf,Howard I. Hurtig,Leslie M. Shaw,Murray Grossman,John Q. Trojanowski +16 more
TL;DR: Higher antemortem CSF t-tau/Aβ1-42 and lower Aβ1/42 levels are predictive of increasing cerebral AD and SYN pathology, which may identify patients with LBD vulnerable to cortical SYn pathology who may benefit from both SYN and AD-targeted disease-modifying therapies.
Journal ArticleDOI
The mTOR pathway is activated in glial cells in mesial temporal sclerosis
Alexander A. Sosunov,Xiaoping Wu,Robert A. McGovern,David G. Coughlin,Charles B. Mikell,Robert R. Goodman,Guy M. McKhann +6 more
TL;DR: The findings suggest that the astroglial “scar” in sclerotic MTLE has active, ongoing cellular changes, and targeting mTOR in MTLE may provide new pathways for the medical therapy of epilepsy.
Journal ArticleDOI
Pathological Influences on Clinical Heterogeneity in Lewy Body Diseases
TL;DR: It is proposed that Alzheimer's disease copathology is one of several likely pathological contributors to clinical heterogeneity of Lewy body disorders, and that such pathology can be assessed in vivo.