Preliminary evidence that negative symptom severity relates to multilocus genetic profile for dopamine signaling capacity and D2 receptor binding in healthy controls and in schizophrenia

Andrey · November 26, 2016, 2:32pm

ncbi.nlm.nih.gov

Preliminary evidence that negative symptom severity relates to multilocus genetic profile for dopamine signaling capacity and D2 receptor binding in healthy controls and in schizophrenia.

SA Eisenstein, R Bogdan, L Chen, SM Moerlein, KJ Black, JS Perlmutter, T Hershey and DM Barch, Journal of psychiatric research, Mar 2017

Deficits in central, subcortical dopamine (DA) signaling may underlie negative symptom severity, particularly anhedonia, in healthy individuals and in schizophrenia. To investigate these relationships, we assessed negative symptoms with the Schedule for the Assessment of Negative Symptoms and the Brief Negative Symptom Scale (BNSS) and self-reported anhedonia with the Scales for Physical and Social Anhedonia (SPSA), Temporal Experience of Pleasure Scale, and Snaith-Hamilton Pleasure Scale in 36 healthy controls (HC), 27 siblings (SIB) of individuals with schizophrenia, and 66 individuals with schizophrenia or schizoaffective disorder (SCZ). A subset of participants (N = 124) were genotyped for DA-related polymorphisms in genes for DRD4, DRD2/ANKK1, DAT1, and COMT, which were used to construct biologically-informed multi-locus genetic profile (MGP) scores reflective of subcortical dopaminergic signaling. DA receptor type 2 (D2R) binding was assessed among a second subset of participants (N = 23) using PET scans with the D2R-selective, non-displaceable radioligand (N-[11C]methyl)benperidol. Higher MGP scores, reflecting elevated subcortical dopaminergic signaling capacity, were associated with less negative symptom severity, as measured by the BNSS, across all participants. In addition, higher striatal D2R binding was associated with less physical and social anhedonia, as measured by the SPSA, across HC, SIB, and SCZ. The current preliminary findings support the hypothesis that subcortical DA function may contribute to negative symptom severity and self-reported anhedonia, independent of diagnostic status.

In a nutshell, they are saying that D2 is implicated in the pathophysiology of negative symptoms, especially anhedonia. This is old news, but somehow I feel refreshed because it sounds like something can be done with the available technology, whereas if there had been a case of disrupted neural networks, we would have had to wait many years before a viable treatment emerges.

far_cry0 · November 26, 2016, 2:44pm

yes…this stuff are really complicated…!!!

I think this is a case of disruption between neural network …!!!
Cuz they are still not able to find any effective treatment to solve this freaking mystery…it looks like dead horror to me…!!! NO way we have to wait some 20 to 30yrs by then I’ll be 60yrs…!!! it doesn;t matter i will fight for American presidency …and make love to some beautiful white ■■■■■ cuz they know the cut…!!! middle finger to our fate and destiny …!!! news never makes me positive this days…and drugs doesn;t work… HEy @Andrey how are u …just don;t read it…take care…!!

Andrey · November 26, 2016, 3:09pm

LOL @far_cry0 you don’t do things by half measures, do you…

far_cry0 · November 26, 2016, 3:17pm

See Andrey neither my med works neither i have any aspiration toward future …its due to Sz…!!!
So i make fun of nearly everything …I am Dead,what can i say…@Andrey don’t take anything personally i just wanted to appreciate u for Ur contribution,and i know ur are cool and handsome as always…!!! Cuz my Damaged mind just don’t Dream.!!

far_cry0 · November 26, 2016, 3:17pm

Means…?? like not understanding the situation…!!

Andrey · November 26, 2016, 3:22pm

You don’t do things by half measure = you want to do great things and go all out.