[Cognitive aging in chronic psychotic patients]. / Vieillissement cognitif des psychotiques chroniques.

OBJECTIVE: The cognitive aging of psychotic patients is still poorly apprehended and sometimes wrongly compared with demential or pseudo-demential deterioration. We studied the impact of chronic psychosis on cognitive performance in the elderly. PATIENTS AND METHODS: We estimated cognitive performance in two groups of 15 patients each among persons on old-age pensions or living in geriatric nursing homes. One group included patients who had already showed dissociative or non-dissociative chronic psychosis and the other group persons with no previous psychotic signs. Cognitive estimations were made on the basis of Folstein's Mini Mental State (MMS) score and Signoret's Battery of Cognitive Efficacy (BEC 96). Results obtained in the two groups were compared with the Mann and Whitney non-parametric test. RESULTS: The psychiatric patients showed a significant deficiency compared with the others for memory and executive functions and also a much broader range of scores on the BEC96 that demonstrated deficiency among the psychiatric patients. DISCUSSION: Though these findings must be interpreted with caution, they do demonstrate a trend similar to that observed in young schizophrenics and also to that of the cognitive performances observed in older schizophrenics and demented subjects. Patients with dissociated or non-dissociated psychotic disorders show an apparent relative cognitive deficiency irrespective of age. The psychotic elderly appear to exhibit a cognitive clash much more than a simple pseudo-demential deficiency.

A new point mutation in the prion protein gene at codon 210 in Creutzfeldt-Jakob disease.

We screened 16 cases of sporadic Creutzfeldt-Jakob disease (CJD) and 28 healthy control subjects to detect possible polymorphisms in their prion protein gene (PRNP). The molecular analysis of the PRNP coding sequence was performed using denaturing gradient gel electrophoresis of polymerase chain reaction products and direct sequencing. We identified (1) a silent mutation at codon 177 in a healthy individual, (2) a codon 200 glutamate-to-lysine substitution in a 48-year-old CJD-affected Libyan Jew, and (3) a G-to-A point substitution at codon 210, leading a valine-to-isoleucine change, in a 63-year-old French CJD patient. This new mutation occurs in a highly conserved part of the PRNP coding sequence, close to the known CJD-associated codon 200 mutation, and might be linked to a symptomatologic and neuropathologic pattern of typical sporadic CJD. This mutation was also present in a sister of the patient who died at the age of 67 without neurologic symptomatology.