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Basic Science and Pathogenesis.

Zehu Sheng1, Ming Chen2, Jin Zhang3

  • 1Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, Chongqing, China.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Elevated cerebrospinal fluid (CSF) Leucine-rich repeat kinase 2 (LRRK2) levels are linked to Alzheimer's disease (AD) pathology and neurodegeneration. TREM2-related microglial activation may mediate LRRK2's role in AD progression.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Genetics

Background:

  • Leucine-rich repeat kinase 2 (LRRK2) is present in brain cells, but its specific role in Alzheimer's disease (AD) and neuroinflammation is not fully understood.
  • Investigating LRRK2's involvement is crucial for understanding AD pathogenesis.

Purpose of the Study:

  • To explore the association between cerebrospinal fluid (CSF) LRRK2 levels and AD biomarkers.
  • To investigate the role of LRRK2 in neuroinflammation and neurodegeneration pathways in AD.
  • To examine the mediating effect of TREM2 in the relationship between LRRK2 and neurodegeneration.

Main Methods:

  • Analysis of 716 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) and 87 from the Parkinson's Progression Markers Initiative (PPMI).
  • Measurement of CSF LRRK2 levels, LRRK2 genotypes, AD core pathology biomarkers, microglial activation, and axonal injury.
  • Application of various statistical models, including regression, mediation, and structural equation modeling, to analyze the data.

Main Results:

  • Higher CSF LRRK2 levels were observed in participants with positive tau pathology in both ADNI and PPMI cohorts.
  • CSF LRRK2 levels significantly correlated with phosphorylated tau (p-Tau), total tau (t-Tau), and neurofilament light chain (NfL) levels.
  • TREM2-dependent pathways mediated the link between LRRK2 and neurodegeneration markers (NfL) in ADNI, while p-Tau partially mediated this relationship in PPMI.

Conclusions:

  • CSF LRRK2 promotes tau-associated synaptic neurodegeneration in Alzheimer's disease.
  • TREM2-related microglial activation appears to be a significant factor in the neurodegenerative process driven by LRRK2.