M
Melissa J. Alldred
Researcher at Nathan Kline Institute for Psychiatric Research
Publications - 45
Citations - 2904
Melissa J. Alldred is an academic researcher from Nathan Kline Institute for Psychiatric Research. The author has contributed to research in topics: Basal forebrain & Cholinergic neuron. The author has an hindex of 24, co-authored 43 publications receiving 2365 citations. Previous affiliations of Melissa J. Alldred include Pennsylvania State University & New York University.
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Journal ArticleDOI
The GDP-GTP Exchange Factor Collybistin: An Essential Determinant of Neuronal Gephyrin Clustering
Kirsten Harvey,Ian Duguid,Melissa J. Alldred,Sarah Beatty,H. E. Ward,Nicholas H. Keep,Sue E. Lingenfelter,Brian Pearce,Johan Lundgren,Michael John Owen,Trevor G. Smart,Bernhard Lüscher,Mark I. Rees,Mark I. Rees,Robert J. Harvey +14 more
TL;DR: The characterization of several new variants of collybistin are reported, which are created by alternative splicing of exons encoding an N-terminal src homology 3 (SH3) domain and three alternate C termini (CB1, CB2, and CB3).
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Microarray Analysis of Hippocampal CA1 Neurons Implicates Early Endosomal Dysfunction During Alzheimer's Disease Progression
Stephen D. Ginsberg,Stephen D. Ginsberg,Melissa J. Alldred,Melissa J. Alldred,Scott E. Counts,Anne M. Cataldo,Rachael L. Neve,Ying Jiang,Ying Jiang,Joanne Wuu,Moses V. Chao,Elliott J. Mufson,Ralph A. Nixon,Ralph A. Nixon,Shaoli Che,Shaoli Che +15 more
TL;DR: The hypothesis that neuronal endosomal dysfunction is associated with preclinical AD is supported and increased endocytic pathway activity, driven by elevated rab GTPase expression, may result in long-term deficits in hippocampal neurotrophic signaling and represent a key pathogenic mechanism underlying AD progression.
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The γ2 Subunit of GABAA Receptors Is a Substrate for Palmitoylation by GODZ
Cheryl A. Keller,Xu Yuan,Patrizia Panzanelli,Michelle L. Martin,Melissa J. Alldred,Marco Sassoè-Pognetto,Bernhard Lüscher +6 more
TL;DR: GODZ-mediated palmitoylation represents a novel posttranslational modification that is selective forγ subunit-containing GABAA receptor subtypes, a mechanism that is likely to be important for regulated trafficking of these receptors in the secretory pathway.
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Autophagy flux in CA1 neurons of Alzheimer hippocampus: Increased induction overburdens failing lysosomes to propel neuritic dystrophy.
Matteo Bordi,Martin J. Berg,Panaiyur S. Mohan,Corrinne M. Peterhoff,Melissa J. Alldred,Shaoli Che,Stephen D. Ginsberg,Ralph A. Nixon +7 more
TL;DR: It is proposed that sustained induction of autophagy in the face of progressively declining lysosomal clearance of substrates explains the uncommonly robust autophagic pathology and neuritic dystrophy implicated in AD pathogenesis.
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Distinct γ2 Subunit Domains Mediate Clustering and Synaptic Function of Postsynaptic GABAA Receptors and Gephyrin
TL;DR: A novel mechanism involved in targeting of GABAA receptors and gephyrin to inhibitory synapses is pointed to in γ2 subunit mutant neurons.