The significance of the Calbindin‐D in Alzheimer’s disease

Abstract

AbstractBackgroundAlzheimer’s disease is a heterogeneous, progressive, and devastating neurodegenerative disease. In addition to the accumulation of Aβ and tau, neuropathological processes in the early stage of AD are accompanied by calcium dysregulation, which might cause the loss of synapses and then dysfunctions of the neural network. Calbindin‐D is abundant throughout the central nervous system (CNS) and one of the neuronal protective factors, also involved in calcium homeostasis. It has been reported that the depletion of Calbindin‐D in AD transgenic mice brain elicited significant alterations in apoptosis, synaptic transmission, and cytoskeleton organization. Despite of the reduced Calbindin expression in the brains of mice and patients with AD, still the role of this protein in AD‐related dysfunction is tested. To obtain better insights into the pathological significance of the protein we assesed the concentarion of Calbindin‐D in cerebrospinal fluid of patients with AD and non‐demented controls.MethodThe study group included 34 subjects: patients with AD and controls without cognitive impairments. The cerebrospinal fluid (CSF) concentrations of tested proteins were measured with the use of multiplexing technique.ResultThe CSF concentrations of Calbindin‐D were elevated in AD patients in comparison to non‐demented controls. Additionally, the CSF levels of Calbindin‐D positively correlated with tau as well as phTau181, and negatively with MMSE in the whole study group.ConclusionOur preliminary study indicates a potential role of Calbindin‐D in the development of AD, although the question, whether this protein can be useful in clinical practice of dementia requires further examination.