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Grants > Exploring the Origins of Tau Pathology in the Human Brainstem Locus Ceruleus Updated On: Jan. 20, 2025
Alzheimer's Disease Research Grant

Exploring the Origins of Tau Pathology in the Human Brainstem Locus Ceruleus

Tau
a headshot of Dr. Morris

Principal Investigator

Meaghan Morris, MD, PhD

Johns Hopkins University School of Medicine

Baltimore, MD, USA

About the Research Project

Program

Alzheimer's Disease Research

Award Type

Standard

Award Amount

$296,426

Active Dates

July 01, 2023 - June 30, 2026

Grant ID

A2023004S

Goals

The aim of this project is to track the origins of tau accumulation and its buildup in the brain over time.

Summary

Tau buildup in the brain starts somewhere, and Meaghan Morris, MD, PhD, and her colleagues will use cutting-edge molecular detection tools to characterize these origins. Tau is one of two key proteins associated with Alzheimer’s disease, and its buildup inside nerve cells in the brain is linked to the cognitive symptoms of the condition and its progression.

For this work, researchers will examine brain samples from 100 people without dementia and across a range of ages. They hope to define the time, location, and molecules involved in the earliest moments that tau starts accumulating in the Locus Ceruleus prior to spreading through the brain. By focusing on the origin story of tau accumulation and spread, they hope to offer a window into the origins of Alzheimer’s disease itself.

Unique and Innovative

This study is innovative in that it is investigating factors associated with the earliest accumulation and spread of tau pathology in human brain. While most studies focus on tau in after it has spread to other brain regions, this study focuses on the factors surrounding the origins of tau pathology with the goal of providing insight into the earliest stages of pathology formation in aging and Alzheimer’s disease.

Foreseeable Benefits

Our study is designed to provide insight into the early mechanisms of tau accumulation and spread in the human brain. This insight will advance our understanding of the origins of pathology in aging and Alzheimer’s disease, and could potentially generate new areas of investigation into preventing tau accumulation in spread in humans as a means of preventing neurodegeneration in Alzheimer’s disease.