Neurogranin: A novel biomarker of Alzheimer’s disease

神经颗粒素 生物标志物 脑脊液 突触可塑性 神经科学 海马体 医学 疾病 认知功能衰退 内科学 心理学 肿瘤科 化学 痴呆 信号转导 受体 生物化学 蛋白激酶C
作者
Maciej Dulewicz,Agnieszka Kulczyńska-Przybik,Aleksandra Klimkowicz‐Mrowiec,Joanna Pera,Renata Borawska,Agnieszka Słowik,Barbara Mroczko
出处
期刊:Alzheimers & Dementia [Wiley]
卷期号:17 (S5) 被引量:1
标识
DOI:10.1002/alz.051279
摘要

Abstract Background Alzheimer’s disease (AD) is a progressive, incurable and fatal neurodegenerative disorder characterized by continuing cognitive decline. Early deficits of memory and other cognitive functions has closely related to synaptic loss in AD. Neurogranin (Ng) is a small protein located in postsynaptic neurons, dendrites and spines in brain structures like the hippocampus. Ng plays an crucial role in synaptic plasticity and long‐term potentiation mediated by calcium and calmodulin signalling pathway, which is essential to memory and learning functions. Considering the above mentioned facts, it seems that Ng can be novel biomarker of synaptic injury. The purposes of our investigation were the quantitive assessment of Ng levels in the CSF of AD patients and comparison with classical biomarkers of AD. Method The cerebrospinal fluid (CSF) levels of neurogranin and classical AD biomarkers, such as Aβ‐42, Aβ‐42/Aβ‐40, hTau and pTau181 were assessed by immunoenzyme assays. The study included 15 patients with AD and 15 non‐demented controls. Result The significantly higher concentration of Ng in cerebrospinal fluid of AD patients compared to non‐demented controls was observed. The CSF level of neurogranin was positively correlated with hTau and pTau181 and negatively with Aβ‐42/Aβ‐40 ratio. Conclusion The Ng is a crucial indicator of synaptopathy in the AD.Our results suggest that Ng is a promising biomarker for AD, however, further studies on larger group patients are needed. Acknowledgement: The study was conducted with the use of equipment purchased by the Medical University of Białystok as part of the RPOWP 2007‐2013 funding, Priority I, Axis 1.1, contract No. UDA‐RPPD.01.01.00‐20001/15‐00 dated 26 and project № POWR.03.02.00‐00‐I051/16 from European Union funds, POWER 2014‐2020, grant № 04/IMSD/G/2019
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