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Does Platelet Transcriptome Dysregulation Across the Lewy Body Continuum Mirror Neuronal Dysfunction?

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|November 27, 2025
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Platelets reveal distinct RNA signatures in neurodegenerative diseases like dementia with Lewy bodies (DLB) and idiopathic REM sleep behavior disorder (IRBD). This study shows platelets as accessible biomarkers for alpha-synucleinopathies.

Keywords:
Alzheimer’s diseaseParkinson’s diseaseRNA sequencingdementia with Lewy bodiesdifferential gene expressionidiopathic REM sleep behavior disorderplatelet transcriptome

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Area of Science:

  • Neuroscience
  • Genomics
  • Hematology

Background:

  • Platelets are multifunctional cells involved in hemostasis, immune regulation, inflammation, and neurodegeneration.
  • Alpha-synucleinopathies, including dementia with Lewy bodies (DLB) and Parkinson disease (PD), are complex neurodegenerative disorders.
  • Idiopathic REM sleep behavior disorder (IRBD) is an early sign of alpha-synucleinopathies.

Purpose of the Study:

  • To investigate disease-specific transcriptomic signatures in platelets from patients with IRBD, DLB, PD, Alzheimer disease (AD), and healthy controls (CTRLs).
  • To explore the role of platelet RNA profiles in the pathogenesis and progression of alpha-synucleinopathies.

Main Methods:

  • RNA-sequencing (RNA-Seq) profiling of platelets from patient cohorts and healthy controls.
  • Differential expression analysis (DEA) to identify transcriptomic changes.
  • Analysis of RNA class distribution, including messenger RNAs (mRNAs) and long non-coding RNAs (lncRNAs).

Main Results:

  • Platelets from DLB patients showed a reduced proportion of lncRNAs, indicating potential RNA regulation impairment.
  • IRBD platelets exhibited the highest number of disease-specific lncRNAs, with many Y-linked, correlating with male predominance in alpha-synucleinopathies.
  • Extensive transcriptomic remodeling was observed in IRBD and DLB, affecting RNA processing, cytoskeletal organization, and platelet activation pathways.
  • PD and AD showed minimal transcriptomic changes, possibly due to disease heterogeneity.

Conclusions:

  • Platelet transcriptomic profiles offer insights into disease-specific molecular alterations in alpha-synucleinopathies.
  • Progressive impairment of platelet activation and signaling in DLB may mirror neuronal dysfunction.
  • Platelets serve as accessible biomarkers for early and disease-stage-specific molecular changes in neurodegenerative conditions.