ArticleJournal of neuropathology and experimental neurology2012
Increased expression of TrkB and Capzb2 accompanies preserved cognitive status in early Alzheimer disease pathology.
Article in Journal of neuropathology and experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Plasma Concentrations of Neurofilament Light Chain Protein and Brain-Derived Neurotrophic Factor as Consistent Biomarkers of Cognitive Impairment in Alcohol Use Disorder.International journal of molecular sciences · 2023Article
- Investigation of the Molecular Role of Brain-Derived Neurotrophic Factor in Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- Evaluation of neurotrophic factors and education level as predictors of cognitive decline in alcohol use disorder.Scientific reports · 2021Article
- Traceable stimulus-dependent rapid molecular changes in dendritic spines in the brain.Scientific reports · 2020Article
- Serum pro-BDNF levels correlate with phospho-tau staining in Alzheimer's disease.Neurobiology of aging · 2020Article
- The Role of Brain-Derived Neurotrophic Factor in the Pathophysiology of Psychiatric and Neurological Disorders.Journal of psychiatry and psychiatric disorders · 2017Article
- Associations between social relationship measures, serum brain-derived neurotrophic factor, and risk of stroke and dementia.Alzheimer's & dementia (New York, N. Y.) · 2017Article
- Neurotrophic factors in Alzheimer's and Parkinson's diseases: implications for pathogenesis and therapy.Neural regeneration research · 2017Review
- Integral Characterization of Defective BDNF/TrkB Signalling in Neurological and Psychiatric Disorders Leads the Way to New Therapies.International journal of molecular sciences · 2017Review
- Genetic variants specific to aging-related verbal memory: Insights from GWASs in a population-based cohort.PloS one · 2017Article
- Article
- BDNF trafficking and signaling impairment during early neurodegeneration is prevented by moderate physical activity.IBRO reports · 2016Article
- Brain-Derived Neurotrophic Factor in Alzheimer's Disease: Risk, Mechanisms, and Therapy.Molecular neurobiology · 2015Article
- The involvement of BDNF, NGF and GDNF in aging and Alzheimer's disease.Aging and disease · 2015Review
- Hippocampal proNGF signaling pathways and β-amyloid levels in mild cognitive impairment and Alzheimer disease.Journal of neuropathology and experimental neurology · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB) may influence brain reserve, the ability of the brain to tolerate pathological changes without significant decline in function. Here, we explore whether a specifically vulnerable population of human neurons shows a compensatory response to the neuropathological changes of Alzheimer disease (AD) and whether that response depends on an upregulation of the BDNF pathway. We observed increased neuronal TrkB expression associated with early-stage AD pathology (Braak and Braak stages I-II) in hippocampal CA1 region samples from cognitively intact Framingham Heart Study subjects (n = 5) when compared with cognitively intact individuals with no neurofibrillary tangles (n = 4). Because BDNF/TrkB signaling affects memory formation and retention through modification of the actin cytoskeleton, we examined the expression of actin capping protein β2 (Capzb2), a marker of actin cytoskeleton reorganization. Capzb2 expression was also significantly increased in CA1 hippocampal neurons of cognitively intact subjects with early-stage AD pathology. Our data suggest that increased expression of TrkB and Capzb2 accompanies adequate brain reserve in the initial stages of AD pathology. In subsequent stages of AD, the higher levels of TrkB and Capzb2 expression achieved may not be sufficient to prevent cognitive decline.
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