V
Vanda A. Lennon
Researcher at Mayo Clinic
Publications - 11
Citations - 6655
Vanda A. Lennon is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Neuromyelitis optica & Optic neuritis. The author has an hindex of 8, co-authored 11 publications receiving 6081 citations. Previous affiliations of Vanda A. Lennon include University of Rochester.
Papers
More filters
Journal ArticleDOI
A serum autoantibody marker of neuromyelitis optica : distinction from multiple sclerosis
Vanda A. Lennon,Dean M. Wingerchuk,Thomas J. Kryzer,Sean J. Pittock,C. F. Lucchinetti,Kazuo Fujihara,Ichiro Nakashima,Brian G. Weinshenker +7 more
TL;DR: NMO-IgG is a specific marker autoantibody of neuromyelitis optica and binds at or near the blood-brain barrier that distinguishes neuromyleitis opticas from multiple sclerosis.
Journal ArticleDOI
Revised diagnostic criteria for neuromyelitis optica
TL;DR: Revised diagnostic criteria for definite neuromyelitis optica (NMO) that require optic neuritis, myelitis, and at least two of three supportive criteria: MRI evidence of a contiguous spinal cord lesion 3 or more segments in length, onset brain MRI nondiagnostic for multiple sclerosis, or NMO-IgG seropositivity.
Journal ArticleDOI
Pathogenic potential of IgG binding to water channel extracellular domain in neuromyelitis optica
Shannon R. Hinson,Sean J. Pittock,C. F. Lucchinetti,Shanu F. Roemer,J. P. Fryer,Thomas J. Kryzer,Vanda A. Lennon +6 more
TL;DR: NMO patients’ serum IgG has a selective pathologic effect on cell membranes expressing aquaporin-4, and targeting astrocytic processes around nodes of Ranvier could initiate demyelination.
Journal ArticleDOI
Aquaporin-4–binding autoantibodies in patients with neuromyelitis optica impair glutamate transport by down-regulating EAAT2
Shannon R. Hinson,Shanu F. Roemer,C. F. Lucchinetti,James P. Fryer,Thomas J. Kryzer,Jayne L. Chamberlain,Charles L. Howe,Sean J. Pittock,Vanda A. Lennon +8 more
TL;DR: It is demonstrated that exposure to NMO patient serum and active complement compromises the membrane integrity of CNS-derived astrocytes and initiates several potentially neuropathogenic mechanisms: complement activation, AQP4 and EAAT2 down-regulation, and disruption of glutamate homeostasis.
Journal ArticleDOI
Paraneoplastic antibodies coexist and predict cancer, not neurological syndrome.
TL;DR: The autoantibody profiles observed in patients with paraneoplastic disorders imply the targeting of multiple onconeural antigens and predict the patient's neoplasm, but not a specific neurological syndrome.