Neurotrophic factor strategies for the treatment of Alzheimer disease

Toshitaka Nabeshima, Kiyofumi Yamada

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Cholinergic neurons in the nucleus basalis of Meynert are reduced early in the course of Alzheimer disease, and the dysfunction of cholinergic neurons is believed to be primarily responsible for cognitive deficits in the disease. Nerve growth factor has a trophic effect on cholinergic neurons and therefore may have some beneficial effects on the cognitive impairment observed in patients with Alzheimer disease. Experimental studies demonstrated that a continuous infusion of nerve growth factor into the cerebroventricle prevents cholinergic neuron atrophy after axotomy or associated with normal aging and ameliorates cognition impairment in these animals. A clinical study in three patients with Alzheimer disease revealed, however, that a long-term intracerebroventricular infusion of nerve growth factor may have certain potentially beneficial effects, but the continuous intracerebroventricular route of administration is also associated with negative side effects that appear to outweigh the positive effects. Several other strategies have been suggested to provide neurotrophic support to cholinergic neurons. In this article, we review the neurotrophic factor strategies for the treatment of Alzheimer disease.

Original languageEnglish
Pages (from-to)S39-S46
JournalAlzheimer Disease and Associated Disorders
Volume14
Issue numberSUPPL. 1
DOIs
Publication statusPublished - 06-07-2000

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Cholinergic Neurons
Nerve Growth Factors
Alzheimer Disease
Nerve Growth Factor
Basal Nucleus of Meynert
Intraventricular Infusions
Therapeutics
Axotomy
Cognition
Atrophy

All Science Journal Classification (ASJC) codes

  • Clinical Psychology
  • Gerontology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health

Cite this

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Neurotrophic factor strategies for the treatment of Alzheimer disease. / Nabeshima, Toshitaka; Yamada, Kiyofumi.

In: Alzheimer Disease and Associated Disorders, Vol. 14, No. SUPPL. 1, 06.07.2000, p. S39-S46.

Research output: Contribution to journalArticle

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