AI Article Synopsis

  • The text refers to a correction made to an article identified by the DOI (Digital Object Identifier) 10.1371/journal.pone.0187305.
  • Corrections are typically made to address errors or updates in previously published research.
  • The DOI system helps in easily locating academic papers and their corrections.

Article Abstract

[This corrects the article DOI: 10.1371/journal.pone.0187305.].

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6438471PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0214340PLOS

Publication Analysis

Top Keywords

correction absence
4
absence anti-hypocretin
4
anti-hypocretin receptor
4
receptor autoantibodies
4
autoantibodies post
4
post pandemrix
4
pandemrix narcolepsy
4
narcolepsy cases
4
cases [this
4
[this corrects
4

Similar Publications

Background: Increased uptake on Tau positron-emission tomography (PET) is sometimes observed in the absence of amyloid β accumulation. This A-T+ PET profile might represent primary age-related tauopathy (PART), an amyloid β-independent 3R/4R tauopathy observed in aging brains. Although A-T+ individuals have been shown to follow a different cognitive trajectory compared to A-T- and A+T+ individuals, it remains unknown how they differ in terms of plasma biomarkers.

View Article and Find Full Text PDF

Background: Establishing practical and effective diagnostic pathways for people with cognitive impairment is a crucial international research priority. Traditional (late-phase) analysis of an amyloid-beta (Aβ) PET scan (∼90 minutes after radiotracer injection) provides important information about the presence/absence of underlying Alzheimer's pathology, but no information about brain metabolism/perfusion. Recent work suggests that amyloid-beta PET tracer uptake shortly after injection ('early-phase') closely reflects brain metabolism and perfusion.

View Article and Find Full Text PDF

Biomarkers.

Alzheimers Dement

December 2024

Imperial College London, London, UK.

Background: Diabetes is associated with an increased risk of developing neurodegenerative conditions, including Alzheimer's disease. Abnormal insulin signalling can lead to impaired phosphorylation of protein kinase B and activation of phosphatidylinositol 3-kinase, resulting in hyperphosphorylation of tau and activation of inflammatory pathways. However, people living with diabetes commonly exhibit comorbid cardiovascular risk, which are also linked with cognitive decline.

View Article and Find Full Text PDF

Biomarkers.

Alzheimers Dement

December 2024

Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

Background: The clinical role and potential mechanisms of the choroid plexus (ChP) in Alzheimer's disease (AD) remains unclear.

Method: This prospective cohort study enrolled 607 participants [110 healthy controls (HCs), 269 mild cognitive impairment (MCI), and 228 AD dementia] from the Chinese Imaging, Biomarkers, and Lifestyle study between January 1, 2021, and December 31, 2022. Relationship between ChP volume and the cerebrospinal fluid (CSF) pathological hallmarks (Aβ, Aβ, Aβ, tTau, and pTau), neuropsychological tests [Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), Neuropsychiatric Inventory (NPI), and Activities of Daily Living (ADL) scores], and multimodal neuroimaging measures were analyzed using partial Spearman's correlation.

View Article and Find Full Text PDF

Biomarkers.

Alzheimers Dement

December 2024

School of Medicine & Public Health, University of Wisconsin-Madison, Madison, WI, USA.

Background: The timing of neurodegeneration in relation to the onset of Alzheimer's disease pathology is not fully known. This study examined the association of longitudinal atrophy derived from T1-weighted MRI with 1) cerebrospinal fluid (CSF) amyloid-tau (AT) groupings and 2) Pittsburgh compound B (PiB) PET-derived estimates of amyloid duration among cognitively unimpaired (CU) individuals.

Method: CU participants in the Wisconsin Registry for Alzheimer's Prevention and Wisconsin Alzheimer's Disease Research Center (N = 297) underwent longitudinal MRI, APOE genotyping, and lumbar puncture to determine CSF Aβ42/40 (A) and pTau181 (T) concentration at baseline using in-house cutoffs.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!