Journal
NEUROBIOLOGY OF DISEASE
Volume 132, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2019.104540
Keywords
Alzheimer's disease; Brain-derived neurotrophic factor; Microarray; Mild cognitive impairment; Neuritic plaques; Neurofibrillary tangles; TrkB; Negative binomial model
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Funding
- National Institutes of Health [PO1 AG014449, RO1 AG043375, PO1 AG107617, R01 NS21072, R01 AG025970, P30 AG010161, P30 AG053769]
- Alzheimer's Association
- Barrow and Beyond at the Barrow Neurological Institute
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Introduction: Downregulation of brain-derived neurotrophic factor (BDNF) and its cognate neurotrophin receptor, TrkB, were observed during the progression of dementia, but whether the Alzheimer's disease (AD) pathological lesions diffuse plaques, (DPs), neuritic plaques (NPs), and neurofibrillary tangles (NFTs) are related to this alteration remains to be clarified. Methods: Negative binomial (NB) regressions were performed using gene expression data accrued from a single population of CA1 pyramidal neurons and regional hippocampal dissections obtained from participants in the Rush Religious Orders Study (RROS). Results: Downregulation of Bdnf is independently associated with increased entorhinal cortex NPs. Downregulation of TrkB is independently associated with increased entorhinal cortex NFTs and CA1 NPs during the progression of AD. Discussion: Results indicate that BDNF and TrkB dysregulation contribute to AD neuropathology, most notably hippocampal NPs and NFTs. These data suggest attenuating BDNF/TrkB signaling deficits either at the level of BDNF, TrkB, or downstream of TrkB signaling may abrogate NPs and/or NFTs.
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