Cognitive conditions of pathologically confirmed dementia with Lewy bodies and Parkinson's disease with dementia.

The relationship between dementia with Lewy bodies (DLB) and Parkinson's disease with dementia (PDD) has been insufficiently described, and it is still problematic. Twenty-nine cases of DLB and 10 cases of PDD were investigated in the present study. DLB cases disclosed a significantly older disease onset and shorter disease duration than PDD cases (p<0.01 each). However, they showed no significant difference in dementia onset or dementia duration (p>0.05 each). Motor symptoms (parkinsonism) were suspected as the cause of the younger disease onset in PDD cases. Compared with 10 age-matched cases of definite Alzheimer's disease, both 19 DLB cases and 6 PDD cases had significantly better scores in the final test of mini-mental state examination (MMSE) and revised version of Hasegawa's Dementia Scale (HDSR) within 12 months before death, although no significant differences between DLB and PDD were indicated. DLB and PDD were suspected to show cognitive impairment of similar severity in the terminal stage. They would thus be difficult to classify as completely different entities.

Specific binding of 125I-hippocampal cholinergic neurostimulating peptide (HCNP) to rat brain membranes: characterization and regional distribution.

An undecapeptide-hippocampal cholinergic neurostimulating peptide (HCNP), originally purified from young rat hippocampus, enhances cholinergic phenotype development in the medial septal nucleus in vitro. To survey and characterize the HCNP receptor within the central nervous system, we used iodinated HCNP as a labeled ligand. In preliminary experiments, [125I]HCNP binding was highest in the crude P2 membrane fraction, so all subsequent experiments were performed using this fraction. The binding was saturable and reversible, and unlabeled ligand inhibited it. Scatchard analysis of the concentration-dependent saturation of binding indicated a single population of non-interacting sites with K(d) 4.0+/-0.7 nM and B(max) 10.7+/-3.8 pmol/mg protein. Dissociation experiments revealed a dissociation constant (K(-1)) of 0.07 min(-1). Inhibition experiments using HCNP and its shorter peptide fragments suggested that the active binding site resided close to the peptide's C-terminal sequence. Since [125I]HCNP binding was found in crude P2 membrane fractions from animals at all ages examined, HCNP may also perform important functional roles in the adult brain. Further, the predominant distribution of the receptor in the P2 membrane fraction, and the similarity in distribution patterns between the binding site and HCNP-precursor protein mRNA expression suggest that the peptide exerts its functions in the vicinity of the dendrites of the neurons that produce it.