Abnormal changes of brain cortical anatomy and the association with plasma MicroRNA107 level in amnestic mild cognitive impairment

Tao Wang, Feng Shi, Yan Jin, Weixiong Jiang, Dinggang Shen, Shifu Xiao

Research output: Contribution to journalArticle

7 Citations (Scopus)

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.

Original languageEnglish
Article number112
JournalFrontiers in Aging Neuroscience
Volume8
Issue numberMAY
DOIs
Publication statusPublished - 2016

Fingerprint

Anatomy
Brain
Language
Messenger RNA
Emotions
Episodic Memory
Amyloid beta-Protein Precursor
Cognitive Dysfunction
Short-Term Memory
Alzheimer Disease
Pathology
Phenotype
Light
Polymerase Chain Reaction
Enzymes
Genes

Keywords

  • Alzheimer's disease
  • Amnestic mild cognitive impairment
  • Biological markers
  • Genetics
  • Surface-based morphometry

ASJC Scopus subject areas

  • Ageing
  • Cognitive Neuroscience

Cite this

Abnormal changes of brain cortical anatomy and the association with plasma MicroRNA107 level in amnestic mild cognitive impairment. / Wang, Tao; Shi, Feng; Jin, Yan; Jiang, Weixiong; Shen, Dinggang; Xiao, Shifu.

In: Frontiers in Aging Neuroscience, Vol. 8, No. MAY, 112, 2016.

Research output: Contribution to journalArticle

@article{5af9b00ca51e4ef68b6f09b22ecefb56,
title = "Abnormal changes of brain cortical anatomy and the association with plasma MicroRNA107 level in amnestic mild cognitive impairment",
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.",
keywords = "Alzheimer's disease, Amnestic mild cognitive impairment, Biological markers, Genetics, Surface-based morphometry",
author = "Tao Wang and Feng Shi and Yan Jin and Weixiong Jiang and Dinggang Shen and Shifu Xiao",
year = "2016",
doi = "10.3389/fnagi.2016.00112",
language = "English",
volume = "8",
journal = "Frontiers in Aging Neuroscience",
issn = "1663-4365",
publisher = "Frontiers Research Foundation",
number = "MAY",

}

TY - JOUR

T1 - Abnormal changes of brain cortical anatomy and the association with plasma MicroRNA107 level in amnestic mild cognitive impairment

AU - Wang, Tao

AU - Shi, Feng

AU - Jin, Yan

AU - Jiang, Weixiong

AU - Shen, Dinggang

AU - Xiao, Shifu

PY - 2016

Y1 - 2016

N2 - 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.

AB - 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.

KW - Alzheimer's disease

KW - Amnestic mild cognitive impairment

KW - Biological markers

KW - Genetics

KW - Surface-based morphometry

UR - http://www.scopus.com/inward/record.url?scp=84974653221&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84974653221&partnerID=8YFLogxK

U2 - 10.3389/fnagi.2016.00112

DO - 10.3389/fnagi.2016.00112

M3 - Article

AN - SCOPUS:84974653221

VL - 8

JO - Frontiers in Aging Neuroscience

JF - Frontiers in Aging Neuroscience

SN - 1663-4365

IS - MAY

M1 - 112

ER -