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Dalton James Surmeier

Researcher at Northwestern University

Publications -  43
Citations -  3161

Dalton James Surmeier is an academic researcher from Northwestern University. The author has contributed to research in topics: Medium spiny neuron & Parkinson's disease. The author has an hindex of 20, co-authored 43 publications receiving 2652 citations.

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Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy

Jose A. Obeso, +44 more
- 01 Sep 2017 - 
TL;DR: This multiple‐author article provides a historical state‐of‐the‐art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease.
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Recurrent Collateral Connections of Striatal Medium Spiny Neurons Are Disrupted in Models of Parkinson's Disease

TL;DR: Recurrent collateral connections between MSNs are not random but rather differentially couple D1 and D2 MSNs, potentially contributing to pathological alterations in MSN activity patterns and psychomotor symptoms in Parkinson's disease models.
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Corticostriatal and Thalamostriatal Synapses Have Distinctive Properties

TL;DR: Differences in release probability and short-term synaptic plasticity suggest that corticostriatal and thalamostRIatal projection systems code information in temporally distinct ways, constraining how they regulate striatal circuitry.
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The L-type channel antagonist isradipine is neuroprotective in a mouse model of Parkinson's disease

TL;DR: Analysis revealed that isradipine produced a dose-dependent sparing of DA fibers and cell bodies at concentrations achievable in humans, suggesting that is Radipine is a potentially viable neuroprotective agent for PD.
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The role of calcium and mitochondrial oxidant stress in the loss of substantia nigra pars compacta dopaminergic neurons in Parkinson's disease.

TL;DR: The hypothesis that the primary factor driving neurodegenerative changes in PD is the metabolic stress created by Ca²⁺ entry is examined, particularly in the face of genetic or environmental factors that compromise oxidative defenses or proteostatic competence.