# MECHANISM OF B-AMYLOID NEUROTOXICITY IN THE RAT BRAIN

> **NIH NIH R01** · WHITTIER INSTITUTE FOR DIABETES & ENDOC · 1992 · $128,043

## Abstract

Intriguing data from other laboratories have shown evidence of acute
effects of solubilized P protein and related fragments in vitro and in vivo
in the rat brain.  As discussed below, it is difficult to assess the
physiological significance of these short term effects with solubilized
peptides which have never been measured in human brain and how they may
relate to the complex, insoluble amyloid deposits known to occur in AD
brain.  In contrast, we have investigated the long-term fate of Alzheimer's
amyloid cores injected into rat hippocampus and observed neuron loss,
Alz-50 and ubiquitin immunoreactivity, and amyloid phagocytosis and
migration to vessel walls (Preliminary studies).  We now propose to extend
and refine this work using progressively more complex synthetic amyloid
deposits to investigate the role of specific molecular and cellular
elements in plaque pathogenesis.  In particular, in addition to putative
neurotoxic effects, we propose to explore the interaction between synthetic
amyloid deposits and heparin binding growth factors and their relationships
to cellular elements involved in AD.

## Key facts

- **NIH application ID:** 3122640
- **Project number:** 5R01AG010685-02
- **Recipient organization:** WHITTIER INSTITUTE FOR DIABETES & ENDOC
- **Principal Investigator:** SALLY ANN FRAUTSCHY
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1992
- **Award amount:** $128,043
- **Award type:** 5
- **Project period:** 1991-09-29 → 1994-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3122640

## Citation

> US National Institutes of Health, RePORTER application 3122640, MECHANISM OF B-AMYLOID NEUROTOXICITY IN THE RAT BRAIN (5R01AG010685-02). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3122640. Licensed CC0.

---

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