A total of 1,081 adults without dementia (375 healthy subjects and 706 individuals with mild cognitive impairment) were recruited from the Alzheimer's Disease Neuroimaging Initiative (ADNI) to test the influence of BDNFVal66Met polymorphism on cognitive impairment, brain structure atrophy, and change in the levels of CSF biomarkers.
Additionally, there were no significant differences in serum BDNF levels between patients with AD and MCI (eight studies, <i>n</i> = 906) and between MCI and HC (nine studies, <i>n</i> = 5090).
Although Val66Met polymorphisms were not associated with the cross-sectional diagnoses of MCI or AD, the presence of Met-BDNF allele was associated with a higher risk of disease-progression in patients with MCI (OR=3.0 CI(95%) [1.2-7.8], P=0.02).
Coincident with these phenomena, brain derived neurotrophic factor (BDNF) and its precursor molecule, proBDNF, are reduced in the MCI cortex, potentially depriving CBF neurons of additional trophic factor support.
CSF concentration of BDNF, Abeta(42) and total tau were measured in 128 cognitively normal adults (Normals), 21 patients with Alzheimer's disease (AD), and nine patients with Mild Cognitive Impairment.
CSF of elderly subjects with mild cognitive impairment shows more oxidative and trophic changes that are characterized by reduction of BDNF content, glutathione-S-transferase activity, and antioxidant potential.
DNA Methylation and Tag SNPs of the BDNF Gene in Conversion of Amnestic Mild Cognitive Impairment into Alzheimer's Disease: A Cross-Sectional Cohort Study.
Elevation of Peripheral BDNF Promoter Methylation Predicts Conversion from Amnestic Mild Cognitive Impairment to Alzheimer's Disease: A 5-Year Longitudinal Study.
Evaluation of hippocampal volume and serum brain-derived neurotrophic factor as potential diagnostic markers of conversion from amnestic mild cognitive impairment to Alzheimer disease: A STROBE-compliant article.
Glycogen synthase kinase (GSK)-3β and brain-derived neurotrophic factor (BDNF) play vital roles in both mild cognitive impairment (MCI) and type 2 diabetes mellitus (T2DM).
In the present study, the mRNA and protein expression level of BDNF was detected in serum, and cerebrospinal fluid (CSF) of patients with mild cognitive impairment (MCI), dementia of Alzheimer's type (DAT), and hippocampus in APP/PS1 mice.
Increased serum BDNF levels after administering DW2009 may provide preliminary insight into the underlying effects of cognitive improvement, which suggests the importance of the gut-brain axis in ameliorating cognitive deficits in MCI.
Increasing levels of S100B, platelet-derived growth factor-AA (PDGF-AA), brain-derived neurotrophic factor (BDNF), and sRAGE were associated with decreased odds of mild neurocognitive disorder (n = 22) or HIV-associated dementia (n = 15) compared with normal function (n = 30) or asymptomatic neurocognitive impairment (n = 11).
Positive effect of mental training on the cognitive parameters, parallel with BDNF elevation, suggests that mental training is a more useful, safe, and persistent strategy to attenuate the progression of MCI probably via BDNF elevation, but the effect size is relatively small elevation.
The mild cognitive impairment/Alzheimer's disease cohort showed a longitudinal decline in entorhinal thickness in BDNF Met carriers compared to Val/Val in APOE E4 carriers, with effect sizes ranging from medium to large.