Author/Authors :
Mahdavi, Meisam Department of Clinical Biochemistry - School of Medicine - Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran , Karima, Saeed Department of Clinical Biochemistry - School of Medicine - Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran , Rajaei, Shima Department of Clinical Biochemistry - School of Medicine - Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran , Aghamolaii, Vajihe Department of Psychiatry - School of Medicine - Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran , Ghahremani, Hossein Department of Clinical Biochemistry - School of Medicine - Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran , Ataei, Reza Department of Clinical Biochemistry - School of Medicine - Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran , Sepasi Tehrani, Hessam Department of Clinical Research, HealthWeX Co., Canada , Mahmoodi Baram, Somayeh Department of Clinical Biochemistry - School of Medicine - Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran , Tafakhori, Abbas Department of Neurology - School of Medicine - Iranian Center of Neurological Research - Neuroscience Institute - Imam Khomeini Hospital - Tehran University of Medical Sciences, Tehran, Iran , Safarpour Lima, Behnam Department of Neurology - School of Medicine - Imam Hossein Hospital - Shahid Beheshti University of Medical Science, Tehran, Iran , Shateri, Somayeh Department of Clinical Biochemistry - School of Medicine - Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran , Fatemi, Hamid Department of Clinical Research, HealthWeX Co., Canada , Mokhtari, Farzad Department of Clinical Research, HealthWeX Co., Canada , Nikzameer, Abdolrahim Department of Clinical Biochemistry - School of Medicine - Shahid Beheshti University of Medical Sciences (SBMU), Tehran, Iran , Yarhosseini, Amir Department of Psychiatry - School of Medicine - Roozbeh Hospital, Tehran University of Medical Sciences, Tehran, Iran , Gorji, Ali Department of Neurology and Department of Neurosurgery - Westfälische Wilhelms-Universität Münster, Münster, Germany
Abstract :
Alzheimer’s disease (AD) is the main cause of the neurodegenerative disorder, which is not detected unless the cognitive deficits are manifested. An early prediagnostic specific biomarker preferably detectable in plasma and hence non-invasive is highly sought-after. Various hypotheses refer to AD, with amyloid-beta (Aβ) being the most studied hypothesis and inflammation being the most recent theory wherein pro-and anti-inflammatory cytokines are the main culprits. Materials and Methods: In this study, the cognitive performance of AD patients (n=39) was assessed using mini-mental state examination (MMSE), AD assessment scale-cognitive subscale (ADAS-cog), and clinical dementia rating (CDR). Their neuropsychiatric symptoms were evaluated through neuropsychiatric inventory–questionnaire (NPI-Q). Moreover, plasma levels of routine biochemical markers, pro-/anti-inflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin-1 α (IL-1α), IL-1β, IL-2, IL-4, IL-6, IL-8, IL-12p70, IL-10, Interferon-gamma, chemokines, including prostaglandin E2 (PGE-2), monocyte chemoattractant protein-1, interferon gamma-induced protein 10, Aβ peptide species (42, 40) and Transthyretin (TTR) were measured. Results: Our results revealed that Aβ 42/40 ratio and TTR were correlated (r=0.367, P=0.037). IL-1α was directly correlated with ADAS-cog (r=0.386, P=0.017) and Aβ 40 (r=0.379, P=0.019), but was inversely correlated with IL-4 (r=-0.406, P=0.011). Negative correlations were found between MMSE and PGE2 (r=-0.405, P=0.012) and TNF-α/ IL-10 ratio (r=-0.35, P=0.037). CDR was positively correlated with both PGE2 (r=0.358, P=0.027) and TNF-α (r=0.416, P=0.013). There was a positive correlation between NPI-caregiver distress with CDR (r=0.363, P=0.045) and ADAS-cog (r=0.449, P=0.019). Conclusion: Based on the observed correlation between IL-1α, as a clinical moiety, and ADAS-cog, as a clinical manifestation of AD, anti-IL-1α therapy in AD could be
suggested.
