# GALANIN IN ALZHEIMER'S DISEASE

> **NIH NIH R01** · RUSH UNIVERSITY MEDICAL CENTER · 1993 · $147,073

## Abstract

The overall objective of this proposal is to gain a more complete
understanding of the pathologic alterations which occur between galanin
containing interneurons and their processes within the cholinergic basal
forebrain in Alzheimer's (AD).  This relationship needs to be examined in
human material, and cannot be accurately modeled in nonhumans, since we
have previously demonstrated a dramatic species difference in the cellular
distribution of galanin-containing profiles in basal forebrain of monkeys
and humans.  Since galanin is inhibitory to acetylcholine, it has been
hypothesized that hyperinnervation by galanin containing neurites upon
nucleus basalis cholinergic neurons in AD may play a key role in the
degenerative process(es) underlying cholinergic cell dysfunction in this
disorder.  To further characterize the relationship between galanin and the
cholinergic basal forebrain in AD, we will determine 1) whether the
reported hyperinnervation by galanin of nucleus basalis neurons also occurs
in the septal/diagonal band complex of the basal forebrain in AD; 2)
whether there is an increase in galanin-containing synapses upon
cholinergic basal forebrain neurons in AD; 3) whether the embryonic
development of galanin-containing basal forebrain efferents is similar to
that seen in AD; 4) whether the enhanced galanin-containing input upon
cholinergic basal forebrain neurons in AD is due to an increased number of
cells expressing galanin mRNA or whether there is an increase in the amount
of galanin mRNA being produced in a stable number of neurons.  The planned
studies will utilize immunohistochemistry using a polyclonal galanin
antibody, galanin mRNA in situ hybridization, and immunoelectron
microscopy.

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 AD.  Furthermore, these data my
suggest avenues for the development of new pharmacological therapies as a
means of retarding intellectual deterioration in dementia.

## Key facts

- **NIH application ID:** 3122591
- **Project number:** 5R01AG010668-03
- **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:** 1993
- **Award amount:** $147,073
- **Award type:** 5
- **Project period:** 1991-09-29 → 1995-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3122591

## Citation

> US National Institutes of Health, RePORTER application 3122591, GALANIN IN ALZHEIMER'S DISEASE (5R01AG010668-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3122591. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*