Cognitive deficits in individuals with methamphetamine use disorder: A meta-analysis

2018 ◽  
Vol 80 ◽  
pp. 154-160 ◽  
Author(s):  
Stéphane Potvin ◽  
Julie Pelletier ◽  
Stéphanie Grot ◽  
Catherine Hébert ◽  
Alasdair M. Barr ◽  
...  
2021 ◽  
Vol 89 (9) ◽  
pp. S148-S149
Author(s):  
Alexandre Guerin ◽  
Yvonne Bonomo ◽  
Kiymet Bozaoglu ◽  
Brian Dean ◽  
Andrew Lawrence ◽  
...  

Author(s):  
Jochen Seitz ◽  
Katharina Bühren ◽  
Georg G. von Polier ◽  
Nicole Heussen ◽  
Beate Herpertz-Dahlmann ◽  
...  

Objective: Acute anorexia nervosa (AN) leads to reduced gray (GM) and white matter (WM) volume in the brain, which however improves again upon restoration of weight. Yet little is known about the extent and clinical correlates of these brain changes, nor do we know much about the time-course and completeness of their recovery. Methods: We conducted a meta-analysis and a qualitative review of all magnetic resonance imaging studies involving volume analyses of the brain in both acute and recovered AN. Results: We identified structural neuroimaging studies with a total of 214 acute AN patients and 177 weight-recovered AN patients. In acute AN, GM was reduced by 5.6% and WM by 3.8% compared to healthy controls (HC). Short-term weight recovery 2–5 months after admission resulted in restitution of about half of the GM aberrations and almost full WM recovery. After 2–8 years of remission GM and WM were nearly normalized, and differences to HC (GM: –1.0%, WM: –0.7%) were no longer significant, although small residual changes could not be ruled out. In the qualitative review some studies found GM volume loss to be associated with cognitive deficits and clinical prognosis. Conclusions: GM and WM were strongly reduced in acute AN. The completeness of brain volume rehabilitation remained equivocal.


2021 ◽  
Vol 224 (2) ◽  
pp. S401-S402
Author(s):  
Marcela Smid ◽  
Amanda A. Allshouse ◽  
Kristine Campbell ◽  
Michelle P. Debbink ◽  
Adam G. Gordon ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Akhil Sharma ◽  
Arman Harutyunyan ◽  
Bernard L. Schneider ◽  
Anna Moszczynska

AbstractThere is no FDA-approved medication for methamphetamine (METH) use disorder. New therapeutic approaches are needed, especially for people who use METH heavily and are at high risk for overdose. This study used genetically engineered rats to evaluate PARKIN as a potential target for METH use disorder. PARKIN knockout, PARKIN-overexpressing, and wild-type young adult male Long Evans rats were trained to self-administer high doses of METH using an extended-access METH self-administration paradigm. Reinforcing/rewarding properties of METH were assessed by quantifying drug-taking behavior and time spent in a METH-paired environment. PARKIN knockout rats self-administered more METH and spent more time in the METH-paired environment than wild-type rats. Wild-type rats overexpressing PARKIN self-administered less METH and spent less time in the METH-paired environment. PARKIN knockout rats overexpressing PARKIN self-administered less METH during the first half of drug self-administration days than PARKIN-deficient rats. The results indicate that rats with PARKIN excess or PARKIN deficit are useful models for studying neural substrates underlying “resilience” or vulnerability to METH use disorder and identify PARKIN as a novel potential drug target to treat heavy use of METH.


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