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Adrienne K. Mehalow
Researcher at Howard Hughes Medical Institute
Publications - 4
Citations - 2920
Adrienne K. Mehalow is an academic researcher from Howard Hughes Medical Institute. The author has contributed to research in topics: Complement system & Synapse. The author has an hindex of 4, co-authored 4 publications receiving 2489 citations.
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Journal ArticleDOI
The classical complement cascade mediates CNS synapse elimination.
Beth Stevens,Nicola J. Allen,Luis E. Vazquez,Gareth R. Howell,Karen S. Christopherson,Navid Nouri,Kristina D. Micheva,Adrienne K. Mehalow,Andrew D. Huberman,Benjamin K. Stafford,Alexander Sher,Alan Litke,John D. Lambris,Stephen J. Smith,Simon W. M. John,Ben A. Barres +15 more
TL;DR: It is shown that C1q, the initiating protein in the classical complement cascade, is expressed by postnatal neurons in response to immature astrocytes and is localized to synapses throughout the postnatal CNS and retina, supporting a model in which unwanted synapses are tagged by complement for elimination and suggesting that complement-mediated synapse elimination may become aberrantly reactivated in neurodegenerative disease.
Journal ArticleDOI
CRB1 is essential for external limiting membrane integrity and photoreceptor morphogenesis in the mammalian retina
Adrienne K. Mehalow,Shuhei Kameya,Richard S. Smith,Norman L. Hawes,James M. Denegre,James A. Young,Lesley S Bechtold,Neena B. Haider,Ulrich Tepass,John R. Heckenlively,Bo Chang,Jürgen K. Naggert,Patsy M. Nishina +12 more
TL;DR: Photoreceptor dysplasia and degeneration in Crb1 mutants strongly vary with genetic background, suggesting that the variability in phenotypes of human patients that carry mutations in CRB1 may be due to interactions with background modifiers in addition to allelic variations.
Journal ArticleDOI
GpnmbR150X allele must be present in bone marrow derived cells to mediate DBA/2J glaucoma.
Michael G. Anderson,K. Saidas Nair,Leslie A Amonoo,Adrienne K. Mehalow,Colleen M. Trantow,Sharmila Masli,Simon W. M. John,Simon W. M. John +7 more
TL;DR: It is suggested that affects of Gpnmb on innate immunity influence susceptibility to glaucoma in DBA/2J mice and a role for GPNmb in bone marrow derived lineages is established.
Journal ArticleDOI
Inducible nitric oxide synthase, Nos2 , does not mediate optic neuropathy and retinopathy in the DBA/2J glaucoma model
Richard T. Libby,Gareth R. Howell,Iok-Hou Pang,Olga V. Savinova,Adrienne K. Mehalow,Joseph W. Barter,Richard S. Smith,Abbot F. Clark,Simon W. M. John,Simon W. M. John +9 more
TL;DR: Glaucomatous neurodegeneration in DBA/2J mice does not require NOS2 activity and neither Nos2 deficiency nor aminoguanidine had any detectable affect on the glaucom atous optic nerve damage.