There is little information on the dynamics of BDNF in the CSF in the continuum between healthy aging, MCI and AD. We included 128 older adults (77 with amnestic MCI, 26 with AD and 25 healthy controls). CSF BDNF level was measured by ELISA assay, and AD biomarkers (Aβ42, T-Tau and P-Tau181) were measured using a Luminex xMAP assay. CSF BDNF levels were significantly reduced in AD subjects compared to MCI and healthy controls (p = 0.009). Logistic regression models showed that lower CSF BDNF levels (p = 0.008), lower CSF Aβ42 (p = 0.005) and lower MMSE scores (p = 0.007) are significantly associated with progression from MCI to AD. The present study adds strong evidence of the involvement of BDNF in the pathophysiology of neurodegenerative changes in AD. Interventions aiming to restore central neurotrophic support may represent future therapeutic targets to prevent or delay the progression from MCI to AD.
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http://dx.doi.org/10.1007/s12017-015-8361-y | DOI Listing |
J Neurol
January 2025
Department of Neurology, University Hospital Frankfurt, Frankfurt Am Main, Germany.
Background: BDNF has increasingly gained attention as a key molecule controlling remyelination with a prominent role in neuroplasticity and neuroprotection. Still, it remains unclear how BDNF relates to clinicoradiological characteristics particularly at the early stage of the disease where precise prognosis for the further MS course is crucial.
Methods: BDNF, NfL and GFAP concentrations in serum and CSF were assessed in 106 treatment naïve patients with MS (pwMS) as well as 73 patients with other inflammatory/non-inflammatory neurological or somatoform disorders using a single molecule array HD-1 analyser.
Int J Mol Sci
November 2024
Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833401, Taiwan.
Molecules
November 2024
Laboratory of Cellular and Molecular Pharmacology, Department of Biology, University of British Columbia, Okanagan Campus, Kelowna, BC V1V 1V7, Canada.
Microglia, the brain immune cells, support neurons by producing several established neurotrophic molecules including glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF). Modern analytical techniques have identified numerous phenotypic states of microglia, each associated with the secretion of a diverse set of substances, which likely include not only canonical neurotrophic factors but also other less-studied molecules that can interact with neurons and provide trophic support. In this review, we consider the following eight such candidate cytokines: oncostatin M (OSM), leukemia inhibitory factor (LIF), activin A, colony-stimulating factor (CSF)-1, interleukin (IL)-34, growth/differentiation factor (GDF)-15, fibroblast growth factor (FGF)-2, and insulin-like growth factor (IGF)-2.
View Article and Find Full Text PDFCells
November 2024
The Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences, Instytucka 3 Str., 05-110 Jabłonna, Poland.
Fluctuations in kynurenic acid (KYNA) and brain-derived neurotrophic factor (BDNF) levels in the brain reflect its neurological status. The aim of the study was to investigate the effect of transiently elevated KYNA concentrations in the cerebroventricular circulation on the expression of BDNF and its high-affinity tropomyosin-related kinase receptor B (TrkB) in specific structures of the sheep brain. Intracerebroventricularly cannulated anestrous sheep were subjected to a series of four 30 min infusions of KYNA: 4 × 5 μg/60 μL/30 min (KYNA20, = 6) and 4 × 25 μg/60 μL/30 min (KYNA100, = 6) or a control infusion ( = 6), at 30 min intervals.
View Article and Find Full Text PDFJ Neurochem
January 2025
Alice Lee Centre for Nursing Studies, Yong Loo Lin School of Medicine, National University of Singapore, Singapore City, Singapore.
Sleep is vital for maintaining physical and mental well-being, impacting cognitive functions like memory and learning through neuroplasticity. Sleep disturbances prevalent in neurological and psychiatric disorders exacerbate cognitive decline, imposing societal burdens. Exploring the relationship between sleep and neuroplasticity elucidates the mechanisms influencing cognition, particularly amidst the prevalent sleep disturbances in these clinical populations.
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