Abstract
MicroRNA107 (Mir107) has been thought to relate to the brain structure phenotype of Alzheimer’s disease. In this study, we evaluated the cortical anatomy in amnestic mild cognitive impairment (aMCI) and the relation between cortical anatomy and plasma levels of Mir107 and beta-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1). Twenty aMCI (20 aMCI) and 24 cognitively normal control (NC) subjects were recruited, and T1-weighted MR images were acquired. Cortical anatomical measurements, including cortical thickness (CT), surface area (SA), and local gyrification index (LGI), were assessed. Quantitative RT-PCR was used to examine plasma expression of Mir107, BACE1 mRNA. Thinner cortex was found in aMCI in areas associated with episodic memory and language, but with thicker cortex in other areas. SA decreased in aMCI in the areas associated with working memory and emotion. LGI showed a significant reduction in aMCI in the areas involved in language function. Changes in Mir107 and BACE1 messenger RNA plasma expression were correlated with changes in CT and SA. We found alterations in key left brain regions associated with memory, language, and emotion in aMCI that were significantly correlated with plasma expression of Mir107 and BACE1 mRNA. This combination study of brain anatomical alterations and gene information may shed lights on our understanding of the pathology of AD.Clinical Trial Registration: http://www.ClinicalTrials.gov, identifier NCT01819545.
Highlights
Alzheimer’s disease (AD) is characterized by a progressive decline in cognition and daily function
No significant differences between the groups were observed in age, gender or education, so the effects of age, gender, education level, and brain size were removed in our analysis
The main goal of this study is to investigate changes in cortical anatomy in amnestic mild cognitive impairment (aMCI) patients, especially on cortical thickness (CT), surface area (SA), and local gyrification index (LGI), and to determine any correlation between structural changes and Mir107 and betasite APP cleaving enzyme 1 (BACE1) plasma levels
Summary
Alzheimer’s disease (AD) is characterized by a progressive decline in cognition and daily function. It is the most common form of dementia worldwide. AD is defined by the intracellular accumulation of aggregated and hyperphosphorylated tau protein, the extracellular deposition of amyloid β (Aβ) peptides, and the accumulation of neurofibrillary tangles and amyloid plaques throughout the cortex (De Strooper, 2010; Kandimalla et al, 2013a,b). A widely accepted hypothesis links the major pathology of AD to the generation and subsequent accumulation of Aβ through sequential cleavage of amyloid precursor protein (APP) by betasite APP cleaving enzyme 1 (BACE1) and γ-secretase (Dislich and Lichtenthaler, 2012). Regulation of expression of the proteins involved in this process plays an important role in AD (Bettens et al, 2009)
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