Reply to: “Aberrant GAP43 Gene Expression Is Alzheimer Disease Pathology‐Specific”
- 21 March 2023
- journal article
- letter
- Published by Wiley in Annals of Neurology
- Vol. 93 (5), 1049
- https://doi.org/10.1002/ana.26639
Abstract
No abstract availableThis publication has 11 references indexed in Scilit:
- Association of Presynaptic Loss with Alzheimer's Disease and Cognitive DeclineAnnals of Neurology, 2022
- Elevated CSF GAP‐43 is Alzheimer's disease specific and associated with tau and amyloid pathologyAlzheimer's & Dementia, 2018
- Microglia-Mediated Synapse Loss in Alzheimer's DiseaseJournal of Neuroscience, 2018
- Synaptic Impairment in Alzheimer’s Disease: A Dysregulated SymphonyTrends in Neurosciences, 2017
- Complement and microglia mediate early synapse loss in Alzheimer mouse modelsScience, 2016
- The Intersection of Amyloid Beta and Tau at Synapses in Alzheimer’s DiseaseNeuron, 2014
- Growth-associated protein GAP-43 in the frontal cortex and in the hippocampus in Alzheimer's disease: an immunohistochemical and quantitative studyJournal of Neural Transmission, 2000
- Neurochemical Dissection of Synaptic Pathology in Alzheimer's DiseaseInternational Psychogeriatrics, 1998
- Expression of two neuronal markers, growth-associated protein 43 and neuron-specific enolase, in rat glial cells.Journal of Molecular Medicine, 1997
- Reduced GAP-43 message levels are associated with increased neurofibrillary tangle density in the frontal association cortex (area 9) in Alzheimer's diseaseNeurobiology of Aging, 1992