Journal of neurology, neurosurgery, and psychiatry
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J. Neurol. Neurosurg. Psychiatr. · Mar 2004
Female preclinical presenilin-1 mutation carriers unaware of their genetic status have higher levels of depression than their non-mutation carrying kin.
To study depressive symptoms in preclinical presenilin-1 (PS1) related Alzheimer's disease. ⋯ Depressive symptoms can occur early in the course of PS1 related Alzheimer's disease, at least in women. This supports the hypothesis that depression may occur as a direct result of the neuropathology underlying Alzheimer's disease.
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A proposal that an endogenous benzodiazepine-like agent named endozepine-4 might be responsible for presentations of recurrent stupor has gained wide acceptance. A case of recurrent stupor over two decades is presented with many similarities to previous cases of "endozepine stupor". This case, however, was caused by exogenous benzodiazepine administration and serves as a warning to clinicians to beware of this diagnosis.
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J. Neurol. Neurosurg. Psychiatr. · Mar 2004
Unilateral posterior parietal lobe lesions disrupt kinaesthetic representation of forearm orientation.
To apply the lesion method to assess neuroanatomical substrates for judgments of forearm orientation from proprioceptive cues in humans. ⋯ The findings suggest that the right and left superior and inferior parietal lobules, posterior superior temporal gyri, and premotor areas play a role in defining higher level coordinate systems for specifying orientation of the right and left forearm.
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J. Neurol. Neurosurg. Psychiatr. · Mar 2004
Association study of Notch 4 polymorphisms with Alzheimer's disease.
The NOTCH4 gene is located at 6p21.3, a site shown in several studies to have significant linkage with Alzheimer's disease. ⋯ No association between two NOTCH4 polymorphisms alone and Alzheimer's disease was observed in the three populations, but there was evidence of an increased risk associated with the 5'-UTR CC genotype in epsilon 4 bearers in the United Kingdom. As no functionality for this polymorphism could be determined, it is likely that the interaction is spurious or results from a linkage disequilibrium of this 5'-UTR polymorphism with another marker elsewhere in the 6p21.3 locus.