A
Alexandra B. Nelson
Researcher at University of California, San Francisco
Publications - 38
Citations - 2919
Alexandra B. Nelson is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Optogenetics & Dopamine. The author has an hindex of 18, co-authored 33 publications receiving 2317 citations. Previous affiliations of Alexandra B. Nelson include Gladstone Institutes & University of California, San Diego.
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Journal ArticleDOI
Seizures and Epileptiform Activity in the Early Stages of Alzheimer Disease
Keith A. Vossel,Alexander J. Beagle,Gil D. Rabinovici,Huidy Shu,Huidy Shu,Suzee E. Lee,Georges Naasan,Manu Hegde,Susannah Cornes,Maya L. Henry,Alexandra B. Nelson,William W. Seeley,Michael D. Geschwind,Maria Luisa Gorno-Tempini,Tina Shih,Heidi E. Kirsch,Paul A. Garcia,Bruce L. Miller,Lennart Mucke +18 more
TL;DR: Common clinical features of patients with aMCI- or AD-associated epilepsy included early age at onset of cognitive decline, early incidence of seizures in the disease course, unilateral temporal epileptic foci detected by serial/extended EEG, transient cognitive dysfunction, and good seizure control and tolerability with lamotrigine and levetiracetam.
Journal ArticleDOI
Distinct roles of GABAergic interneurons in the regulation of striatal output pathways.
TL;DR: Surprisingly, it is found that FS interneurons preferentially target direct-pathway MSNs over indirect-pathways MSNs, suggesting a potential mechanism for rapid pathway-specific regulation of striatal output pathways.
Journal ArticleDOI
Reassessing Models of Basal Ganglia Function and Dysfunction
TL;DR: This review summarizes historical models of basal ganglia function, as well as findings supporting or conflicting with these models, while emphasizing recent work in animals and humans directly testing the hypotheses generated by these models.
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Circuit Mechanisms of Parkinson’s Disease
TL;DR: This Review will discuss key clinical features of PD and their basis in neural circuit dysfunction, and review PD-related changes in network activity, subdividing findings into those that touch on the rate, rhythm, or synchronization of neurons.
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Long-Lasting Increases in Intrinsic Excitability Triggered by Inhibition
TL;DR: Firing rate potentiation is a novel form of cellular plasticity that could contribute to motor learning in the vestibulo-ocular reflex and may serve as a complementary mechanism to synaptic plasticity.