Clinical and Environmental Correlates of Serum BDNF: A Descriptive Study with Plausible Implications for AD Research.
Brain derived neurotrophic factor (BDNF) may play a central role in the pathogenesis of Alzheimer's disease (AD) through neurotrophic effects on basal cholinergic neurons. Reduced serum levels of BDND are observed among AD patients and may predict AD risk. Nevertheless, knowledge about factors associated with its levels in blood is lacking.



To identify clinical and demographic correlates of serum BDNF levels.



BDNF was measured from serum collected between 1992-1996 and 1998-2001 in participants from the Original and Offspring cohorts of the Framingham Study, respectively. A cross-sectional analysis was done to evaluate the relationship between clinical measures and BDNF levels using standard linear regression and stepwise models. Analyses were conducted in the total sample and separately in each cohort, and were adjusted for age and sex.



BDNF was measured in 3,689 participants (mean age 65 years, 56% women; 82% Offspring). Cigarette smoking and high total cholesterol were associated with elevated BDNF levels, and history of atrial fibrillation was associated with decreased levels. Elevated BDNF levels were related to greater physical activity and lower Tumor Necrosis Factor-α levels in Offspring. Stepwise models also revealed associations with statin use, alcohol consumption and Apolipoprotein Eε4 genotype.



Serum BDNF correlates with various metabolic, inflammatory and life-style measures which in turn have been linked with risk of AD. Future studies of serum BDNF should adjust for these correlates and are needed to further explore the underlying interplay between BDNF and other factors in the pathophysiology of cognitive impairment and AD.
School of Public Health, University of Haifa, 199 Aba Khoushy Ave., Mount Carmel, Haifa. Israel.
Galit
G
Weinstein
The Framingham Study, Framingham, MA, United States.
Sarah R
SR
Preis
The Department of Biostatistics, Boston University School of Public Health, Boston, MA, United States.
Alexa S
AS
Beiser
The Framingham Study, Framingham, MA, United States.
Bernhard
B
Kaess
The Department of Neurology, Boston University School of Medicine, Boston, MA, United States.
Tai C
TC
Chen
The Department of Neurology, Boston University School of Medicine, Boston, MA, United States.
Claudia
C
Satizabal
The Department of Medicine, Boston University School of Medicine, Boston, MA, United States.
Faisal
F
Rahman
The Department of Epidemiology, Boston University School of Public Health, Boston, MA, Boston, United States.
Emelia J
EJ
Benjamin
The Department of Epidemiology, Boston University School of Public Health, Boston, MA, Boston, United States.
Ramachandran S
RS
Vasan
The Framingham Study, Framingham, MA, United States.
Sudha
S
Seshadri
D000328:Adult; D000544:Alzheimer Disease / Q000097:blood* / Q000175:diagnosis*; D019208:Brain-Derived Neurotrophic Factor / Q000097:blood*; D002097:C-Reactive Protein / Q000378:metabolism; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006710:Homocysteine / Q000097:blood; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D011569:Psychiatric Status Rating Scales; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D019208:Brain-Derived Neurotrophic Factor; D014409:Tumor Necrosis Factor-alpha; D006710:Homocysteine; D002097:C-Reactive Protein
Alzheimer’s disease; Brain-derived neurotrophic factor; cohort studies; cross sectional analysis