The default mode network (DMN) is particularly relevant to Alzheimer's disease (AD) since its structures are vulnerable to deposition of amyloid. Decreased levels of β-amyloid(1-42) (Aβ42) and increased total tau protein (T-tau) and tau phosphorylated at position threonine 181 (P-tau(181p)) in cerebrospinal fluid (CSF) have been established as valid biomarkers for the diagnosis and prognosis of AD. However, the relationship between CSF biomarkers and change in the DMN is still unknown. In this study we investigated the correlation between the functional connectivity within the DMN and the ratio of Aβ42/P-tau(181p) in the CSF. We found that the ratio of Aβ42/P-tau(181p) was moderately positively correlated with the functional connectivity within the DMN in the left precuneus/cuneus. This finding implicates that the brain functional connectivity within DMN is affected by pathological changes at early stage in AD. This may provide a better understanding of AD pathology progression and improve AD diagnosis.
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http://dx.doi.org/10.1038/srep01339 | DOI Listing |
Mol Brain
August 2024
School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Mild Cognitive Impairment (MCI) is a neurological condition characterized by a noticeable decline in cognitive abilities that falls between normal aging and dementia. Along with some biomarkers like GAP-43, Aβ, tau, and P-tau, brain activity and connectivity are ascribed to MCI; however, the link between brain connectivity changes and such biomarkers in MCI is still being investigated. This study explores the relationship between biomarkers like GAP-43, Aβ, tau, and P-tau, and brain connectivity.
View Article and Find Full Text PDFChin Med J (Engl)
July 2021
Department of Neurology, Yantaishan Hospital, Yantai, Shandong 264003, China.
Background: According to the amyloid, tau, neurodegeneration research framework classification, amyloid and tau positive (A+T+) mild cognitive impairment (MCI) individuals are defined as prodromal Alzheimer disease. This study was designed to compare the clinical and biomarker features between A+T+MCI individuals who progressed to progressive MCI (pMCI) and those who remained stable MCI (sMCI), and to identify relevant baseline clinical biomarker and features that could be used to predict progression to dementia within 2 years.
Methods: We stratified 197 A+T+MCI individuals into pMCI (n = 64) and sMCI (n = 133) over 2 years.
J Alzheimers Dis
July 2016
Florey Institute of Neuroscience and Mental Health, The University of Melbourne, VIC, Australia.
Background: The cerebrospinal fluid (CSF) amyloid-β (Aβ)(1-42), total-tau (T-tau), and phosphorylated-tau (P-tau181P) profile has been established as a valuable biomarker for Alzheimer's disease (AD).
Objective: The current study aimed to determine CSF biomarker cut-points using positron emission tomography (PET) Aβ imaging screened subjects from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging, as well as correlate CSF analyte cut-points across a range of PET Aβ amyloid ligands.
Methods: Aβ pathology was determined by PET imaging, utilizing ¹¹C-Pittsburgh Compound B, ¹⁸F-flutemetamol, or ¹⁸F-florbetapir, in 157 AIBL participants who also underwent CSF collection.
PLoS One
May 2016
Neuroscience Therapeutic Area, Janssen Research & Development, LLC, 1125 Trenton-Harbourton Road, Titusville, NJ 08560, United States of America.
Proteolytic fragments of amyloid and post-translational modification of tau species in Cerebrospinal fluid (CSF) as well as cerebral amyloid deposition are important biomarkers for Alzheimer's Disease. We conducted genome-wide association study to identify genetic factors influencing CSF biomarker level, cerebral amyloid deposition, and disease progression. The genome-wide association study was performed via a meta-analysis of two non-overlapping discovery sample sets to identify genetic variants other than APOE ε4 predictive of the CSF biomarker level (Aβ1-42, t-Tau, p-Tau181P, t-Tau:Aβ1-42 ratio, and p-Tau181P:Aβ1-42 ratio) in patients enrolled in the Alzheimer's Disease Neuroimaging Initiative (ADNI) study.
View Article and Find Full Text PDFFront Neurol
July 2015
Reference Center for Biological Markers of Dementia (BIODEM), Institute Born-Bunge, University of Antwerp , Antwerp , Belgium ; Department of Neurology and Memory Clinic, Hospital Network Antwerp (ZNA) Middelheim and Hoge Beuken, Antwerp , Belgium.
The goal of this study is to investigate the value of tau phosphorylated at threonine 181 (P-tau181P) in the Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarker panel for differential dementia diagnosis in autopsy confirmed AD and non-AD patients. The study population consisted of 140 autopsy confirmed AD and 77 autopsy confirmed non-AD dementia patients. CSF concentrations of amyloid-β peptide of 42 amino acids (Aβ1-42), total tau protein (T-tau), and P-tau181P were determined with single analyte ELISA-kits (INNOTEST(®), Fujirebio, Ghent, Belgium).
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