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Walter G, Byrne S, Griffiths O, Hunt G, Soh N, Cleary M, Duffy P, Crawford G, Krabman P, Concannon P, Malhi G. Can young people reliably rate side effects of low-dose antipsychotic medication using a self-report survey?
Lee H-Y, Kim Y-K. Effect of TGF-β1 polymorphism on the susceptibility to schizophrenia and treatment response to atypical antipsychotic agent.
Several studies have suggested that cytokine alterations could be related to the pathophysiology of schizophrenia. Transforming growth factor-beta1 (TGF-β1) is believed to be an important factor in regulation of inflammatory responses and to have anti-inflammatory effects. TGF-β1 also has trophic effects on dopaminergic neurons. We tested the hypothesis TGF-β1 is associated with the pathophysiology of schizophrenia.
The polymorphisms at codon 10 (T869C) and codon 25 (G915C) of TGF-β1 were analysed in 99 schizophrenia patients and 130 normal controls. At baseline and after 8 weeks of treatment, clinical symptoms were evaluated on Positive and Negative Syndrome Scale (PANSS).
None of the subjects were polymorphic at codon 25. However, the C allele at codon 10 was more frequent in schizophrenia (p = 0.05). Although schizophrenia group showed a higher tendency of allele frequency in the subjects with C allele (p = 0.05), the allelic difference did not reach statistical significance after correction for multiple comparisons (p = 0.1).
PANSS scores showed no significant correlation with genotypes. The genotype distribution was not significantly different between responders and non-responders. However, the C allele was more frequent among responders (p = 0.03).
These results suggest that the TGF-β1 polymorphism is associated with therapeutic response to antipsychotics. However, further studies with larger numbers of subjects are needed to confirm the effect of TGF-β1 in schizophrenia.
Stewart G, McGeown WJ, Shanks MF, Venneri A. Anosognosia for memory impairment in Alzheimer's disease.
To investigate whether patients with Alzheimer's disease (AD) were able to alter their awareness of memory deficits after exposure to a memory task.
Thirty normal older adults and 23 mild AD patients participated in the study. Anosognosia was assessed using discrepancies between self- and informant-evaluations of cognitive and functional performance. Participants estimated their performance on the Verbal Paired Associates task at different points in time (before, immediately after the task and after a 1-h delay).
AD patients were generally less able to judge their memory abilities than healthy older adults, and tended to overestimate their task performance beforehand. Their prediction accuracy increased immediately after the task, but after a 1-h delay, they again misjudged their abilities at pretesting accuracy levels. Self-carer discrepancy scores of awareness of deficits in memory and other areas correlated significantly with memory tests but not with other neuropsychological tasks in the assessment, and larger discrepancy scores were associated with poorer performance.
AD patients can monitor their task performance online, but are unable to maintain awareness of their deficits over time. Loss of awareness of memory deficits (or of any other deficits) in early stage AD may indicate damage to a system which updates a personal knowledge base with recent information. Failure to retain this information impedes abstraction from episodic to semantic memory.
Verhoeven WMA, Bon BV, Egger JIM, Hoischen A, Doelman JC. An adult female patient with ring chromosome 21: behavioural phenotype and results of high-resolution molecular characterisation.
A female adult patient with mild to moderate mental retardation and minor dysmorphisms was referred for neuropsychiatric examination because of psychotic and autistic symptoms and impulsive behaviours.
Standardized neuropsychiatric and neuropsychological assessment as well as detailed somatic and neurological examination was performed. For genetic analysis, karyotyping, whole genome array analysis, and high-resolution detailed analysis of chromosome 21 were carried through.
Karyotyping showed a de novo ring chromosome 21: 46,XX,der(21)r(21)(p11q22.3). High-resolution array analysis demonstrated a complex aberration consisting of an interstitial duplication in 21q21.1, an interstitial deletion in 21q22.2q22.3, an interstitial deletion in 21q22.3 and a terminal deletion of 21q22.3. Apart from mild dysmorphisms, visual and auditory impairments, and infertility, no somatic or neurological abnormalities were found. A formal psychiatric diagnosis could not be established. The behavioural problems and the supposed psychiatric symptoms could be related to her disharmonic social cognitive profile. The behaviour normalized after the patient returned to a stable and structured living environment.
High-resolution micro-array analysis techniques are essential to substantiate the genotype–phenotype correlation in patients with r(21) and other genetic disorders. Moreover, the results of this study stress the importance of the recognition of alexithymia as a potential cause for behavioural problems and psychiatric symptoms in patients with mental retardation in general.