# Does Contact Sport Induce Fibrillar Amyloid Deposition in the Brain?

> **NIH NIH R21** · STATE UNIVERSITY NEW YORK STONY BROOK · 2021 · $427,250

## Abstract

PROJECT SUMMARY/ABSTRACT
Repetitive concussive and subconcussive brain trauma, as experienced in contact sports and military
deployment, has been linked to devastating neurodegenerative disease in the long term, such as chronic
traumatic encephalopathy (CTE) and Alzheimers disease (AD), but the mechanisms linking them remain
largely elusive. It is well known that TBI can acutely induce increases in beta amyloid protein via axonal
damage and there is evidence that this can evolve into amyloid plaques, but the magnitude, duration and
implications of this increase have not been well studied in living humans, especially in mild TBI which is the
most common form. The consequences of induced toxic amyloid species are worrisome, especially
considering recent evidence that beta amyloid might directly stimulate production of tau protein via the
adrenergic system, illustrating a new pathway through which amyloid may result in neurotoxicity even if its
elevation is modest and subsequently cleared by normal physiological processes or pharmacological
interventions. While this has enormous implications for AD research, it also raises the tantalizing possibility
that amyloid is an important factor in the risk of neurodegeneration following TBI, perhaps including the mildest
forms to which young athletes and service members are frequently exposed. Fortunately, there are robust and
sensitive ways to measure beta amyloid in the living brain. In Aim 1, we will employ the most validated,
quantitative PET/MR imaging techniques (11C-PiB with arterial input function and compartmental modeling) to
sensitively measure brain levels of amyloid in college contact-sport athletes before and after a season of play.
Our primary hypothesis is that global cortical amyloid distribution volume will be higher after the season. In
Aim 2, we will explore relationships of this measure with related measures of traumatic axonal injury of
associated white matter (using fractional anisotropy with DTI MRI, acquired simultaneously to PET), plasma
biomarkers, and objective exposure variables measured by accelerometer. Although this is a preliminary
mechanistic study, it could lead to vital new directions for diagnostic and preventative approaches across the
full spectrum of TBI severity.

## Key facts

- **NIH application ID:** 10302426
- **Project number:** 1R21NS119948-01A1
- **Recipient organization:** STATE UNIVERSITY NEW YORK STONY BROOK
- **Principal Investigator:** PAUL VASKA
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $427,250
- **Award type:** 1
- **Project period:** 2021-09-22 → 2025-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10302426

## Citation

> US National Institutes of Health, RePORTER application 10302426, Does Contact Sport Induce Fibrillar Amyloid Deposition in the Brain? (1R21NS119948-01A1). Retrieved via AI Analytics 2026-05-27 from https://api.ai-analytics.org/grant/nih/10302426. Licensed CC0.

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