Skip to main content
construction release_alert
Scholars@Duke will be undergoing maintenance April 11-15. Some features may be unavailable during this time.
cancel
Journal cover image

Fiber tract-specific white matter lesion severity Findings in late-life depression and by AGTR1 A1166C genotype.

Publication ,  Journal Article
Taylor, WD; Zhao, Z; Ashley-Koch, A; Payne, ME; Steffens, DC; Krishnan, RR; Hauser, E; MacFall, JR
Published in: Hum Brain Mapp
February 2013

Past work demonstrated that late-life depression is associated with greater severity of ischemic cerebral hyperintense white matter lesions, particularly frontal lesions. However, these lesions are also associated with other neuropsychiatric deficits, so these clinical relationships may depend on which fiber tracts are damaged. We examined the ratio of lesion to nonlesioned white matter tissue within multiple fiber tracts between depressed and nondepressed elders. We also sought to determine if the AGTR1 A1166C and BDNF Val66Met polymorphisms contributed to vulnerability to lesion development in discrete tracts. The 3T structural MR images and blood samples for genetic analyses were acquired on 54 depressed and 37 nondepressed elders. Lesion maps were created through an automated tissue segmentation process and applied to a probabilistic white matter fiber tract atlas allowing for identification of the fraction of the tract occupied by lesion. The depressed cohort exhibited a significantly greater lesion ratio only in the left upper cingulum near the cingulate gyrus (F((1,86)) = 4.62, P = 0.0344), supporting past work implicating cingulate dysfunction in the pathogenesis of depression. In the 62 Caucasian subjects with genetic data, AGTR1 C1166 carriers exhibited greater lesion ratios across multiple tracts including the anterior thalamic radiation and inferior fronto-occipital fasciculus. In contrast, BDNF Met allele carriers exhibited greater lesion ratios only in the frontal corpus callosum. Although these findings did not survive correction for multiple comparisons, this study supports our hypothesis and provides preliminary evidence that genetic differences related to vascular disease may increase lesion vulnerability differentially across fiber tracts.

Duke Scholars

Altmetric Attention Stats
Dimensions Citation Stats

Published In

Hum Brain Mapp

DOI

EISSN

1097-0193

Publication Date

February 2013

Volume

34

Issue

2

Start / End Page

295 / 303

Location

United States

Related Subject Headings

  • Receptor, Angiotensin, Type 1
  • Polymorphism, Single Nucleotide
  • Polymorphism, Genetic
  • Polymerase Chain Reaction
  • Neural Pathways
  • Nerve Fibers, Myelinated
  • Middle Aged
  • Male
  • Magnetic Resonance Imaging
  • Image Processing, Computer-Assisted
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Taylor, W. D., Zhao, Z., Ashley-Koch, A., Payne, M. E., Steffens, D. C., Krishnan, R. R., … MacFall, J. R. (2013). Fiber tract-specific white matter lesion severity Findings in late-life depression and by AGTR1 A1166C genotype. Hum Brain Mapp, 34(2), 295–303. https://doi.org/10.1002/hbm.21445
Taylor, Warren D., Zheen Zhao, Allison Ashley-Koch, Martha E. Payne, David C. Steffens, Ranga R. Krishnan, Elizabeth Hauser, and James R. MacFall. “Fiber tract-specific white matter lesion severity Findings in late-life depression and by AGTR1 A1166C genotype.Hum Brain Mapp 34, no. 2 (February 2013): 295–303. https://doi.org/10.1002/hbm.21445.
Taylor WD, Zhao Z, Ashley-Koch A, Payne ME, Steffens DC, Krishnan RR, et al. Fiber tract-specific white matter lesion severity Findings in late-life depression and by AGTR1 A1166C genotype. Hum Brain Mapp. 2013 Feb;34(2):295–303.
Taylor, Warren D., et al. “Fiber tract-specific white matter lesion severity Findings in late-life depression and by AGTR1 A1166C genotype.Hum Brain Mapp, vol. 34, no. 2, Feb. 2013, pp. 295–303. Pubmed, doi:10.1002/hbm.21445.
Taylor WD, Zhao Z, Ashley-Koch A, Payne ME, Steffens DC, Krishnan RR, Hauser E, MacFall JR. Fiber tract-specific white matter lesion severity Findings in late-life depression and by AGTR1 A1166C genotype. Hum Brain Mapp. 2013 Feb;34(2):295–303.
Journal cover image

Published In

Hum Brain Mapp

DOI

EISSN

1097-0193

Publication Date

February 2013

Volume

34

Issue

2

Start / End Page

295 / 303

Location

United States

Related Subject Headings

  • Receptor, Angiotensin, Type 1
  • Polymorphism, Single Nucleotide
  • Polymorphism, Genetic
  • Polymerase Chain Reaction
  • Neural Pathways
  • Nerve Fibers, Myelinated
  • Middle Aged
  • Male
  • Magnetic Resonance Imaging
  • Image Processing, Computer-Assisted