G
Garrett E. Alexander
Researcher at Johns Hopkins University School of Medicine
Publications - 6
Citations - 7017
Garrett E. Alexander is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Indirect pathway of movement & Basal ganglia. The author has an hindex of 6, co-authored 6 publications receiving 6795 citations.
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Journal ArticleDOI
Functional architecture of basal ganglia circuits: neural substrates of parallel processing
TL;DR: Recent evidence indicating that a parallel functional architecture may also be characteristic of the organization within each individual circuit is discussed, which represents a significant departure from earlier concepts of basal ganglia organization.
Book ChapterDOI
Basal ganglia-thalamocortical circuits: parallel substrates for motor, oculomotor, "prefrontal" and "limbic" functions.
TL;DR: It now appears that at the level of the putamen such inputs remain segregated within the "motor" circuit, and it is difficult to imagine how such functional specificity could be maintained in the absence of strict topographic specificity within the sequential projections that comprise these two circuits.
Book ChapterDOI
Functional organization of the basal ganglia: contributions of single-cell recording studies.
Mahlon R. DeLong,Apostolos P. Georgopoulos,Michael D. Crutcher,S. J. Mitchell,R. T. Richardson,Garrett E. Alexander +5 more
TL;DR: The presence of somatotopic organization in the putamen and globus pallidus, together with known topographic striopallidal connections, suggests that segregated, parallel cortico-subcortical loops subserve 'motor' and 'complex' functions.
Journal ArticleDOI
Necrotizing arteritis and spinal subarachnoid hemorrhage in Sjögren syndrome.
Elaine L. Alexander,Carolyn F. Craft,Carole A. Dorsch,Robert L. Moser,Thomas T. Provost,Garrett E. Alexander +5 more
TL;DR: Anti‐Ro(SSA) antibodies are associated with the occurrence of vasculitis in patients with Sjögren syndrome, which suggests that the spinal arteritis and subarachnoid hemorrhage in this patient may have been directly related to the underlying connective tissue disorder.
Journal ArticleDOI
Congenic autoimmune murine models of central nervous system disease in connective tissue disorders.
TL;DR: Congenic mice of the MRL/Mp strain spontaneously develop an autoimmune connective tissue disease that shares immunological and histopathological features with systemic lupus erythematosus, rheumatoid arthrithritis, and Sjögren's syndrome, and the autoimmune disorder in these mice is accelerated markedly by the recessive gene lpr.