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Meredith Spindler

Researcher at University of Pennsylvania

Publications -  38
Citations -  930

Meredith Spindler is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Medicine & Health care. The author has an hindex of 12, co-authored 29 publications receiving 581 citations. Previous affiliations of Meredith Spindler include Veterans Health Administration.

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National randomized controlled trial of virtual house calls for Parkinson disease.

TL;DR: This study provides Class III evidence that for patients with PD, virtual house calls from a neurologist are feasible and do not significantly change quality of life compared to in-person visits.
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The past, present, and future of telemedicine for Parkinson's disease.

TL;DR: The past, present, and likely future applications of telemedicine to PD are described, including integrated care networks that connect patients to a wide range of providers; education programs that support patients and health care providers; and new research applications that include remote monitoring and remote visits.
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Multimodal evaluation demonstrates in vivo 18 F-AV-1451 uptake in autopsy-confirmed corticobasal degeneration

TL;DR: F-AV-1451 is a PET radioligand that achieves in vivo binding in Alzheimer’s disease (AD) and autoradiographic evidence of binding to paired helical filaments (PHFs) composed of 3-repeat misfolded tau and 4Rtau characteristic of AD histopathology is reported.
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Efficacy of Nilotinib in Patients With Moderately Advanced Parkinson Disease: A Randomized Clinical Trial.

Tanya Simuni, +90 more
- 01 Mar 2021 - 
TL;DR: While nilotinib demonstrated acceptable safety and tolerability in this cohort, the low cerebrospinal fluid exposure, lack of biomarkers effects, and efficacy data trending in the negative direction indicate that further testing ofnilotinib in treatment of Parkinson disease is not warranted.
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CSF tau and β-amyloid predict cerebral synucleinopathy in autopsied Lewy body disorders.

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.