A Homer1 gene variant influences brain white matter structure and lithium effects in bipolar disorder

2017 ◽  
Vol 27 ◽  
pp. S834
Author(s):  
A. Vitali ◽  
E. Mazza ◽  
C. Lorenzi ◽  
S. Poletti ◽  
I. Bollettini ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
White Matter ◽  
Gene Variant ◽  
Brain White Matter

White Matter Microstructure in Bipolar Disorder Is Influenced by the Interaction between a Glutamate Transporter EAAT1 Gene Variant and Early Stress

2018 ◽  
Vol 56 (1) ◽  
pp. 702-710 ◽  
Author(s):  
Sara Poletti ◽  
Irene Bollettini ◽  
Cristina Lorenzi ◽  
Alice Vitali ◽  
Silvia Brioschi ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
White Matter ◽  
Glutamate Transporter ◽  
Gene Variant ◽  
Early Stress ◽  
White Matter Microstructure

scholarly journals GRIN2B Gene and Associated Brain Cortical White Matter Changes in Bipolar Disorder: A Preliminary Combined Platform Investigation

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Carissa Nadia Kuswanto ◽  
Min Yi Sum ◽  
Christopher Ren Zhi Thng ◽  
Yi Bin Zhang ◽  
Guo Liang Yang ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
White Matter ◽  
Diffusion Tensor ◽  
Frontal Region ◽  
White Matter Integrity ◽  
Glutamate Toxicity ◽  
Occipital Region ◽  
Cingulate Gyrus ◽  
White Matter Changes ◽  
Brain White Matter

Abnormalities in glutamate signaling and glutamate toxicity are thought to be important in the pathophysiology of bipolar disorder (BD). Whilst previous studies have found brain white matter changes in BD, there is paucity of data about how glutamatergic genes affect brain white matter integrity in BD. Based on extant neuroimaging data, we hypothesized that GRIN2B risk allele is associated with reductions of brain white matter integrity in the frontal, parietal, temporal, and occipital regions and cingulate gyrus in BD. Fourteen patients with BD and 22 healthy controls matched in terms of age, gender and handedness were genotyped using blood samples and underwent diffusion tensor imaging. Compared to G allele, brain FA values were significantly lower in BD patients with risk T allele in left frontal region (P=0.001), right frontal region (P=0.002), left parietal region (P=0.001), left occipital region (P=0.001), right occipital region (P<0.001), and left cingulate gyrus (P=0.001). Further elucidation of the interactions between different glutamate genes and their relationships with such structural, functional brain substrates will enhance our understanding of the link between dysregulated glutamatergic neurotransmission and neuroimaging endophenotypes in BD.

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