To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Examining neurometabolic abnormalities in critical brain areas in schizophrenia and major depressive disorder (MDD) may help guide future pharmacological interventions including glutamate-modulating treatments.
To measure metabolite concentrations within the anterior cingulate cortex (ACC) and thalamus of people with schizophrenia and people with MDD.
Spectra were acquired from 16 volunteers with schizophrenia, 17 with MDD and 18 healthy controls using magnetic resonance spectroscopy on a 7 Tesla scanner.
In the thalamus, there were lower glycine concentrations in the schizophrenia group relative to control (P=0.017) and MDD groups (P=0.012), and higher glutamine concentrations relative to healthy controls (P=0.009). In the thalamus and the ACC, the MDD group had lower myo-inositol concentrations than the control (P=0.014, P=0.009, respectively) and schizophrenia (P=0.004, P=0.002, respectively) groups.
These results support the glutamatergic theory of schizophrenia and indicate a potential glycine deficiency in the thalamus. In addition, reduced myo-inositol concentrations in MDD suggest its involvement in the disorder.
Thalamic glutamine loss and grey matter reduction suggest
neurodegeneration in first-episode schizophrenia, but the duration is
To observe glutamine and glutamate levels, grey matter volumes and social
functioning in patients with schizophrenia followed to 80 months after
Grey matter volumes and proton magnetic resonance spectroscopy
metabolites in left anterior cingulate and left thalamus were measured in
17 patients with schizophrenia before medication and 10 and 80 months
after diagnosis. Social functioning was assessed with the Life Skills
Profile Rating Scale (LSPRS) at 80 months.
The sum of thalamic glutamate and glutamine levels decreased over 80
months, and correlated inversely with the LSPRS. Thalamic glutamine and
grey matter loss were significantly correlated in frontal, parietal,
temporal and limbic regions.
Brain metabolite loss is correlated with deteriorated social functioning
and grey matter losses in schizophrenia, consistent with
Progressive volumetric changes in the brains of people with schizophrenia have been attributed to a number of factors.
To determine whether glutamatergic changes in patients with schizophrenia correlated with grey-matter losses during the first years of illness.
Left anterior cingulate and thalamic glutamatergic metabolite levels and grey-matter volumes were examined in 16 patients with first-episode schizophrenia before and after 10 months and 30 months of antipsychotic treatment and in 16 healthy participants on two occasions 30 months apart.
Higher than normal glutamine levels were found in the anterior cingulate and thalamus of never-treated patients. Thalamic levels of glutamine were significantly reduced after 30 months. Limited grey-matter reductions were seen in patients at 10 months followed by widespread grey-matter loss at 30 months. Parietal and temporal lobe grey-matter loss was correlated with thalamic glutamine loss.
Elevated glutamine levels in never-treated patients followed by decreased thalamic glutamine and grey-matter loss in connected regions could indicate either neurodegeneration or a plastic response to reduced subcortical activity.
Email your librarian or administrator to recommend adding this to your organisation's collection.