Dimitrios Kapogiannis (United States of America)
National Institute on Aging (NIA/NIH)
Laboratory of Clinical Investigation
Dimitrios Kapogiannis is a Senior Investigator and Chief of the Human Neuroscience Section at the National Institute on Aging and Adjunct Associate Professor at the Department of Neurology at Johns Hopkins University. He earned his Medical Degree from the National and Kapodistrian University of Athens, Greece; completed Neurology Residency at Massachusetts General and Brigham and Women’s Hospitals of Harvard University and a Fellowship in Cognitive and Behavioral Neurology at the National Institute of Neurological Disorders and Stroke, NIH. He has been a pioneer in isolating Extracellular Vesicles (EVs) enriched for brain cell origin from blood and using them to derive biomarkers for neurological and psychiatric diseases and as outcomes for experimental treatments. His research includes basic and translational research focusing on EVs and biomarker discovery for neurodegenerative diseases, especially, Alzheimer’s disease. He also conducts clinical studies investigating the effects of various metabolic interventions on cognitive performance and biomarkers.

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PLASMA NEURONAL-ORIGIN EXTRACELLULAR VESICLES PROVIDE BIOMARKERS FOR COGNITIVE IMPAIRMENT IN PARKINSON’S DISEASE

Session Name
1550 - FLUID BIOMARKERS 4 (ID 215)
Session Type
SYMPOSIUM
Date
Sat, 19.03.2022
Session Time
09:10 AM - 11:25 AM
Room
ONSITE: 131-132
Lecture Time
09:40 AM - 09:55 AM
Presenter

Abstract

Aims

Besides motor symptoms, many individuals with Parkinson’s disease (PD) develop cognitive impairment (PD-CI), mild cognitive impairment (PD-MCI) or dementia (PDD), partly from co-existing Alzheimer’s disease (AD) pathologies and insulin resistance. Biomarkers for PD-CI could improve PD diagnosis and prognosis. We aimed to develop biomarkers distinguishing PD from Control and PD with normal cognition (PD-N) from PD-CI.

Methods

We analyzed plasma samples from 271 participants [103 PD-N, 121 PD-CI (81 PD-MCI, 40 PDD), and 49 Controls]. Extracellular vesicles enriched for neuronal origin (NEVs) were immunocaptured by targeting L1CAM. Biomarkers were quantified using immunoassays for α-synuclein, Aβ42, total tau, pTau181, phosphorylated Tyr-, Ser312- insulin receptor substrate-1 (IRS-1), and phospho-, total- mechanistic target of rapamycin (mTOR).

Results

NEV α-synuclein was lower in PD compared to Controls (p < 0.05) and PD-CI compared to PD-N (p < 0.001) or Controls (p < 0.001). Aβ42 did not differ between groups. pTau181 was higher in PD than Controls (p < 0.05) and PD-CI compared to PD-N (p < 0.05) or Controls (p < 0.01). tTau was not different between groups. pTyr-IRS-1 did not differ between PD and Controls, but was lower in PD-CI compared to PD-N (p < 0.01) and Controls (p < 0.05), and also decreased with increasing motor symptom severity by MDS-UPDRS III (p < 0.01). mTOR was not different between groups, whereas pmTOR trended lower in PD-CI compared to PD-N (p = 0.05).

Conclusions

Findings suggest that both α-synuclein and Tau pathologies and impaired insulin signaling underlie PD-CI. Plasma NEVs biomarkers may inform cognitive prognosis in PD.

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