Complement factor H levels are decreased and correlated with serum C-reactive protein in late-onset Alzheimer's

Guo Lu1, Weihong Liu2, Xinying Huang1

  • 1Dezhou People's Hospital, Department of Neurology, Dezhou, Shandong, China.

Insights

Complement factor H (CFH) levels are decreased in Alzheimer's disease (AD) patients and correlate with C-reactive protein (CRP), but not cognitive scores or BDNF. This suggests CFH may play a role in AD pathogenesis.

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is the leading cause of dementia, yet its underlying pathologies remain unclear.
  • There is a critical need for reliable diagnostic biomarkers for AD.
  • Human complement factor H (CFH) is investigated for its potential role in late-onset AD.

Purpose of the Study:

  • To investigate the clinical significance of human complement factor H (CFH) in patients diagnosed with late-onset Alzheimer's disease.
  • To explore the relationship between CFH serum levels and other biomarkers and cognitive function in AD.

Main Methods:

  • A prospective study involving 187 late-onset AD patients, 100 with mild cognitive impairment (MCI), and 80 healthy controls.
  • Serum levels of CFH, C-reactive protein (CRP), and brain-derived neurotrophic factor (BDNF) were measured using ELISA.
  • Mini-mental state examination (MMSE) scores were assessed for cognitive function evaluation.

Main Results:

  • No significant demographic differences were observed between the groups (age, gender, education).
  • AD patients exhibited significantly lower MMSE scores compared to MCI and healthy controls.
  • Serum levels of CFH, CRP, and BDNF were markedly reduced in AD patients versus controls.

Conclusions:

  • Complement factor H (CFH) serum levels are decreased in patients with late-onset Alzheimer's disease.
  • CFH levels showed a positive correlation with CRP levels but no significant correlation with BDNF or MMSE scores.
  • These findings contribute clinical evidence to the potential involvement of CFH in the pathogenesis of Alzheimer's disease.
Abstract

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