# Extracellular Vesicle treatment and age-related neuropathology in non-human primates

> **NIH NIH R01** · BOSTON UNIVERSITY MEDICAL CAMPUS · 2020 · $702,747

## Abstract

ABSTRACT
Normal aging is characterized by deficits in cognition particularly in the domains of memory (1-6) and executive
function.(1, 2, 7-11) Evidence suggests these changes are not a consequence of widespread cortical neuronal loss,
but rather are attributable to alteration and/or loss of white matter myelin, axons, synapses and dendrites, and
changes in oxidative metabolism and inflammation.(12-18) Further there is growing evidence that accumulation of
pathological Tau and A-Beta are related to age-related cognitive decline, even in the absence of Alzheimer’s
Disease and Related Dementias (ADRD). Thus, one potential therapy, mesenchymal stem cells (MSCs), have
recently received attention as a possible intervention in aging,(19-22) as they are known to suppress inflammation
and facilitate tissue repair and remyelination. (19, 23, 24) Further, we have demonstrated that human umbilical-
derived cells, and MSC-derived extracellular vesicles (EVs), the active product of MSCs, reduce inflammation
and enhance recovery of motor function in non-human primates (NHP) and rodents following cortical injury(25, 26)
and promote axonal growth and myelination in vitro.(27-37) Similarly, EVs have been shown to improve cognitive
deficits in diabetic rats and APP/PS1 mice (model of Alzheimer’s disease).(24, 38, 39) Whether these EV-mediated
beneficial effects can be applied to normal aging and age-related neuropathology in primates is largely unknown.
However, our pilot data show that administration of MSC-EVs in aged female rhesus monkeys decreases A-Beta
deposition. Based on this evidence and our data showing EV-mediated enhancement of recovery after cortical
injury in NHPs, we build upon on our experience over the past three decades (NIH-NIA Program Project
AG00001-34) characterizing cognitive function in the rhesus monkey across the life-span and age-related
changes in the brain (40, 41) to assess the impact of MSC-EVs in our rhesus monkey model of aging. Specifically,
we will investigate the efficacy of EVs to slow or reverse age-related cognitive decline and reduce markers of
inflammation, myelin atrophy, and tau and A-Beta deposition. We will then quantify the effects of EVs on reducing
age-related synaptic dysfunction and changes in electrophysiological properties of neurons. Finally, we will
conduct an in-depth proteomic analysis of treatment and endogenous EVs to establish the profile of the active
biological cargo load responsible for treatment efficacy. This longitudinal, multi-disciplinary study will shed light
on the relationships of neuroinflammatory pathways, myelin damage and ADRD like pathology and cognitive
decline associated with normal aging, and test the efficacy of EVs in ameliorating these age-related deficits in
neural structure and function.

## Key facts

- **NIH application ID:** 10030314
- **Project number:** 1R01AG068168-01
- **Recipient organization:** BOSTON UNIVERSITY MEDICAL CAMPUS
- **Principal Investigator:** TARA L MOORE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $702,747
- **Award type:** 1
- **Project period:** 2020-09-15 → 2025-04-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10030314

## Citation

> US National Institutes of Health, RePORTER application 10030314, Extracellular Vesicle treatment and age-related neuropathology in non-human primates (1R01AG068168-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10030314. Licensed CC0.

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