BDNF-Met polymorphism and amyloid-beta in relation to cognitive decline in cognitively normal elderly: the SCIENCe project

Bosch, Karlijn A. van den; Verberk, Inge M.W.; Ebenau, Jarith L.; Lee, Sven J. van der; Jansen, Iris E.; Prins, Niels D.; Scheltens, Philip; Teunissen, Charlotte E.; Flier, Wiesje M. van der

doi:10.1016/j.neurobiolaging.2021.08.018

Cited by 6 publications

(2 citation statements)

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“…While only few studies examined the effect of BDNF on AD pathology, the literature is consistent in that the relationship between BDNF and memory is dependent on amyloid, but potential effect-modification by APOE is less clear. In in A␤-SCD participants, no increased risk of dementia was found, but combined A␤+ and Val66Met+ did cognitively worse than A␤+ only [8], with similar findings in unimpaired but increased AD risk [11] suggesting a synergistic effect of Met+ and A␤. However, no moderating effect of APOE 4 was found on cognition.…”

Section: Discussionmentioning

confidence: 52%

“…However, so far studies linking BDNF to AD pathophysiology remain inconclusive. Previous studies have shown an association of lower serum BDNF to widespread A␤ 42 in PET studies [6] and faster disease progression in Met carriers, and this effect is magnified by the presence of an Apolipoprotein E (APOE) 4 allele [7,8]. On the other hand, clinically healthy Val-Val individuals showed lower hippocampal volume compared to heterozygotes and with a dose-response effect with the number of APOE 4 alleles [9].…”

Section: Introductionmentioning

confidence: 96%

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Distinct Patterns Link the BDNF Val66Met Polymorphism to Alzheimer’s Disease Pathology

Riphagen

Hooren

Kenis

et al. 2022

JAD

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The brain-derived neurotropic growth factor (BDNF) gene has been linked to dementia, inflammation, and Apolipoprotein E (APOE) ɛ4 status. We used cerebrospinal fluid (CSF) amyloid-β (Aβ)42 and phosphorylated tau (p-tau) to investigate associations with BDNF polymorphisms and modifications by APOE ɛ4 or inflammation in a memory clinic population (n = 114; subjective cognitive decline, mild cognitive impairment, Alzheimer’s disease). We found distinct pathways to Alzheimer’s disease pathology: Val-Met displayed lower CSF-Aβ 42 in APOE ɛ4+ carriers, independent of p-tau, while Val-Val displayed greater p-tau at higher IL-6 and sub-threshold Aβ 42. This may contribute to resolving some inconsistencies in the BDNF literature and provide possible inroads to specific Aβ and tau interventions depending on BDNF polymorphism.

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Section: Discussionmentioning

confidence: 52%