# GALANIN PLASTICITY IN ALZHEIMER'S DISEASE

> **NIH NIH R01** · RUSH UNIVERSITY MEDICAL CENTER · 1992 · $134,306

## Abstract

The overall objective of this proposal is to gain a more complete
understanding of the pathologic alterations which occur between
magnocellular cholinergic neurons and galanin containing interneurons and
their processes within the basal forebrain of human normal aged,
Alzheimer's (AD) and Parkinson's (PD) dementia individuals.  Since galanin
is inhibitory to acetylcholine, it has been hypothesized that
hyperinnervation by galanin containing profiles upon nucleus basalis
cholinergic neurons in AD and PD may play a key role in the degenerative
process(es) underlying cholinergic cell dysfunction in these
neurodegenerative disorders.  To evaluate this hypothesis we will 1)
determine the cellular location of mRNA for galanin synthesis within the
human basal forebrain subfields, 2) determine whether the expression of
galanin mRNA parallels the species difference between human and monkeys we
reported for the peptide galanin within the basal forebrain (36), 3)
determine whether other basal forebrain cell types not currently known to
contain the peptide galanin express its mRNA, 40 determine whether galanin
hyperinnervation to the cholinergic basal forebrain neurons occurs in all
subfields of this region in Alzheimer's and Parkinson's dementia, 5)
determine whether the hyperinnervation of galanin profiles within the
nucleus basalis is accompanied by an over expression of galanin mRNA, and
6) determine whether the basal forebrain hypertrophic galanin containing
profiles innervate ALZ-50 expressing elements.  The planned studies will
utilize immunohistochemistry using a polyclonal galanin antibody, an IgM
mouse monoclonal ALZ-50 antibody and galanin mRNA in situ hybridization.

The data generated from this proposal will provide much needed information
concerning the neurodegenerative events which may play a pivotal role in
basal forebrain cholinergic degeneration in Alzheimer's and Parkinson's
dementias.  Furthermore, these data may suggest avenues for the development
of new pharmacological therapies as a means of retarding intellectual
deterioration in dementia.

## Key facts

- **NIH application ID:** 3123408
- **Project number:** 1R01AG011482-01
- **Recipient organization:** RUSH UNIVERSITY MEDICAL CENTER
- **SAM.gov UEI:** C155UU2TXCP3
- **Principal Investigator:** ELLIOTT Jay MUFSON
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $134,306
- **Award type:** 1
- **Project period:** 1992-09-30 → 1995-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3123408

## Citation

> US National Institutes of Health, RePORTER application 3123408, GALANIN PLASTICITY IN ALZHEIMER'S DISEASE (1R01AG011482-01). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3123408. Licensed CC0.

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