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<p>Alzheimer’s disease (AD) and related dementias (DEM) involve immunological, vascular, and neurological abnormalities. Circulating L1 cell adhesion molecule (L1CAM/CD171)-enriched extracellular vesicles (NEVs), combined with haematological markers, may reflect multisystem changes associated with disease progression. We evaluated 412 individuals: Controls (<i>n</i> = 161), DEM (<i>n</i> = 61), AD (<i>n</i> = 132), mild cognitive impairment (MCI; <i>n</i> = 27), and other neurological disorders (OND; <i>n</i> = 31). Plasma NEVs were enriched using L1CAM immunocapture and quantified by cluster of differentiation 81 (CD81) enzyme-linked immunosorbent assay (ELISA). Acetylcholinesterase (AChE) activity, total vesicle protein, and lipid content were measured. Statistical analyses included non-parametric testing, correlations, and discriminant modeling integrating cognitive scores and haematological parameters such as hemoglobin (Hb), hematocrit (Hct), mean platelet volume (MPV), and leukocyte subsets. NEV concentrations differed significantly (H = 25.7, <i>p</i> &lt; 0.001): controls 49.0, MCI 63.6, AD 32.9, DEM 35.4, and OND 28.3 ng/mL. NEVs were reduced in AD and DEM but relatively elevated in MCI, indicating a possible early compensatory response, although interpretation is limited by the small MCI sample size. AD showed elevated MPV, neutrophil-lymphocyte imbalance, and mild normocytic anaemia. NEVs in AD had higher protein and reduced AChE activity. NEV-MPV correlations reversed across stages (MCI <i>r</i> = -0.42; AD <i>r</i> = 0.45). Classification accuracy reached 74–83%. Integrated NEV and haematologic changes suggest a continuum from early adaptive responses to progressive neurovascular-immune dysregulation during neurodegenerative disease progression. Findings should be interpreted in the context of L1CAM-enriched vesicles and require validation in larger cohorts.</p> Graphical abstract <p></p>

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A combined neuronal extracellular vesicle-haematology panel for clinical stratification of Alzheimer’s disease and dementia

  • 期刊论文

  • 发表日期：

    2026年5月30日

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  • Praveena Ganji,
  • Prasad Rao G,
  • Bala Krishna N,
  • Rajesh V Bendre,
  • Amitabha Ghosh,
  • Subhashani Prabhakar,
  • Rukmini Mridula K,
  • Sasidhar V Manda

摘要

Alzheimer’s disease (AD) and related dementias (DEM) involve immunological, vascular, and neurological abnormalities. Circulating L1 cell adhesion molecule (L1CAM/CD171)-enriched extracellular vesicles (NEVs), combined with haematological markers, may reflect multisystem changes associated with disease progression. We evaluated 412 individuals: Controls (n = 161), DEM (n = 61), AD (n = 132), mild cognitive impairment (MCI; n = 27), and other neurological disorders (OND; n = 31). Plasma NEVs were enriched using L1CAM immunocapture and quantified by cluster of differentiation 81 (CD81) enzyme-linked immunosorbent assay (ELISA). Acetylcholinesterase (AChE) activity, total vesicle protein, and lipid content were measured. Statistical analyses included non-parametric testing, correlations, and discriminant modeling integrating cognitive scores and haematological parameters such as hemoglobin (Hb), hematocrit (Hct), mean platelet volume (MPV), and leukocyte subsets. NEV concentrations differed significantly (H = 25.7, p < 0.001): controls 49.0, MCI 63.6, AD 32.9, DEM 35.4, and OND 28.3 ng/mL. NEVs were reduced in AD and DEM but relatively elevated in MCI, indicating a possible early compensatory response, although interpretation is limited by the small MCI sample size. AD showed elevated MPV, neutrophil-lymphocyte imbalance, and mild normocytic anaemia. NEVs in AD had higher protein and reduced AChE activity. NEV-MPV correlations reversed across stages (MCI r = -0.42; AD r = 0.45). Classification accuracy reached 74–83%. Integrated NEV and haematologic changes suggest a continuum from early adaptive responses to progressive neurovascular-immune dysregulation during neurodegenerative disease progression. Findings should be interpreted in the context of L1CAM-enriched vesicles and require validation in larger cohorts.

Graphical abstract