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Iwase T, Katada E, Matsukawa N, et al. High levels of hippocampal cholinergic neurostimulating peptide (HCNP) in the CSF of some patients with Alzheimer's disease. Eur J Neurol. 1998;5(6):561-569doi: 10.1046/j.1468-1331.1998.560561.x.
Iwase, T., Katada, E., Matsukawa, N., Mitake, S., Ojika, K., Otsuka, Y., & Tsugu, Y. (1998). High levels of hippocampal cholinergic neurostimulating peptide (HCNP) in the CSF of some patients with Alzheimer's disease. European journal of neurology, 5(6), 561-569. https://doi.org/10.1046/j.1468-1331.1998.560561.x
Iwase, et al. "High levels of hippocampal cholinergic neurostimulating peptide (HCNP) in the CSF of some patients with Alzheimer's disease." European journal of neurology vol. 5,6 (1998): 561-569. doi: https://doi.org/10.1046/j.1468-1331.1998.560561.x
Iwase T, Katada E, Matsukawa N, Mitake S, Ojika K, Otsuka Y, Tsugu Y. High levels of hippocampal cholinergic neurostimulating peptide (HCNP) in the CSF of some patients with Alzheimer's disease. Eur J Neurol. 1998 Nov;5(6):561-569. doi: 10.1046/j.1468-1331.1998.560561.x. PMID: 10210891.
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Eur J Neurol. 1998 Nov;5(6):561-569. doi: 10.1046/j.1468-1331.1998.560561.x.

High levels of hippocampal cholinergic neurostimulating peptide (HCNP) in the CSF of some patients with Alzheimer's disease.

European journal of neurology

Iwase, Katada, Matsukawa, Mitake, Ojika, Otsuka, Tsugu

Affiliations

  1. Second Department of Internal Medicine, Medical School, Nagoya City University, Kawasumi, Mizuho-ku, Nagoya 467-8601, Japan.

PMID: 10210891 DOI: 10.1046/j.1468-1331.1998.560561.x

Abstract

Hippocampal cholinergic neurostimulating peptide (HCNP), originally purified from the hippocampus of young rats, enhances the cholinergic development of rat medial septal nuclei in vitro. This report concerns the determination of the HCNP content of the cerebrospinal fluid (CSF) of 173 clinically, and of 22 clinico-pathologically defined patients. A radioimmunoassay was used throughout. The HCNP level was relatively uniform among the clinically defined patients; for almost all non-Alzheimer's patients, the level fell within the range delimited by +/- 2 SD of the mean for all patients taken together, and none of them had a level above this range. By contrast, the early-onset Alzheimer's disease patients could be divided on the basis of their HCNP level into two groups, one with high levels (markedly above the mean +/- 2SD range), and the other with levels similar to those of the other patients. The analysis of the CSF samples obtained postmortem revealed that Group I Alzheimer-type dementia (ATD) patients with clinico-pathologically established diagnoses had a strikingly higher level of HCNP than patients with either Group II ATD or cerebral vascular disease. These results suggest that HCNP is involved in certain pathophysiological alterations associated with dementia, and that its determination may be useful in patient evaluation. Copyright 1998 Lippincott Williams & Wilkins

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