# Contribution of sensorimotor function to risk and pathogenic mechanisms of Alzheimer's disease and related dementias

> **NIH NIH R01** · JOHNS HOPKINS UNIVERSITY · 2020 · $726,100

## Abstract

PROJECT SUMMARY
Alzheimer's disease (AD) is the most common cause of dementia. Underlying pathological and physiological
changes related to the onset and progression of AD are believed to emerge several years prior to clinical
manifestations. Sensory impairments, gait abnormalities, and motor slowing may precede the diagnosis of AD
by a decade or more, presenting the exciting possibility that changes in sensorimotor functioning may act as
early noninvasive biomarkers for AD. Previous work by our group has identified links between cognitive
performance and sensory impairment and gait speed and variability, making them potential preclinical markers
of early AD pathology. We propose to use up to 10 years of existing longitudinal data, and ongoing/new data
collection in approximately 1,000 older adults in the Baltimore Longitudinal Study of Aging (BLSA), to examine
the roles of sensory function, gait speed and variability, and free-living measures of daily physical activity (PA)
as precursors to cognitive impairment. We will also determine the link between sensorimotor measures and
biomarkers of AD pathology, including Aβ deposition using [11C]-Pittsburgh compound B positron emission
tomography, brain atrophy using structural magnetic resonance imaging (MRI), Tau and pTau from cerebrospinal
fluid, and cognitive performance. We will further utilize the rich data resources of the BLSA to develop a
parsimonius prediction model for risk of progression to MCI/AD, and validate its performance in the
Atherosclerosis Risk in Communities (ARIC) study. A better understanding of the associations among
sensorimotor changes, subclinical AD pathology, and cognitive performance may elucidate a high-risk phenotype
that is associated with increased risk of poor cognitive outcomes over time and increase our understanding of
the complex associations among declines in sensory, physical, and cognitive functioning with age. To this end,
future intervention studies of AD prevention might screen for sensorimotor impairments as a high-risk phenotype
reflective of increased risk for developing AD, which could serve as surrogate outcomes in clinical trials.
Moreover, sensorimotor impairments may present feasible and modifiable targets for AD prevention by
identifying critical threshold(s) for implementation of assistive and rehabilitative technologies such as hearing
aids, corrective lenses, surgical or pharmacologic procedures to correct hearing and/or vision impairment (e.g.,
cataract surgery, cochlear implants), and physical therapy/timing and coordination of movement training to
correct gait abnormalities.

## Key facts

- **NIH application ID:** 9858208
- **Project number:** 5R01AG061786-02
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **Principal Investigator:** Yuri Agrawal
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $726,100
- **Award type:** 5
- **Project period:** 2019-02-01 → 2023-11-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9858208

## Citation

> US National Institutes of Health, RePORTER application 9858208, Contribution of sensorimotor function to risk and pathogenic mechanisms of Alzheimer's disease and related dementias (5R01AG061786-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9858208. Licensed CC0.

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