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The CSF p-tau/β-amyloid 42 ratio correlates with brain structure and fibrillary β-amyloid deposition in cognitively unimpaired individuals at the earliest stages of pre-clinical Alzheimer's disease.
Brain Commun
December 2024
Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona 08005, Spain.
CSF concentrations of β-amyloid 42 (Aβ42) and phosphorylated tau (p-tau) are well-established biomarkers of Alzheimer's disease and have been studied in relation to several neuropathological features both in patients and in cognitively unimpaired individuals. The CSF p-tau/Aβ42 ratio, a biomarker combining information from both pathophysiological processes, has emerged as a promising tool for monitoring disease progression, even at pre-clinical stages. Here, we studied the association between the CSF p-tau/Aβ42 ratio with downstream markers of pre-clinical Alzheimer's disease progression including brain structure, glucose metabolism, fibrillary Aβ deposition and cognitive performance in 234 cognitively unimpaired individuals, who underwent cognitive testing, a lumbar puncture, MRI, 18F-fluorodeoxyglucose and 18F-flutemetamol PET scanning.
View Article and Find Full Text PDFFunctional connectivity abnormalities in clinical variants of progressive supranuclear palsy.
Neuroimage Clin
December 2024
Department of Radiology, Mayo Clinic, Rochester, MN, USA.
Progressive supranuclear palsy (PSP) can present with different clinical variants which show distinct, but partially overlapping, patterns of neurodegeneration and tau deposition in a network of regions including cerebellar dentate, superior cerebellar peduncle, midbrain, thalamus, basal ganglia, and frontal lobe. We sought to determine whether disruptions in functional connectivity within this PSP network measured using resting-state functional MRI (rs-fMRI) differed between PSP-Richardson's syndrome (PSP-RS) and the cortical and subcortical clinical variants of PSP. Structural MRI and rs-fMRI scans were collected for 36 PSP-RS, 25 PSP-cortical and 34 PSP-subcortical participants who met the Movement Disorder Society PSP clinical criteria.
View Article and Find Full Text PDFβ-Asarone regulates microglia polarization to alleviate TBI-induced nerve damage via Fas/FasL signaling axis.
Hum Cell
December 2024
Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Jiangxi Hospital, National Reginal Center for Neurological Disease, Honggutan District, No.266 Fenghe North Avenue, Nanchang, 330038, Jiangxi, China.
Acute injury and secondary injury caused by traumatic brain injury (TBI) seriously threaten the health of patients. The purpose of this study was to investigate the role of β-Asarone in TBI-induced neuroinflammation and injury. In this work, the effects of β-Asarone on nerve injury and neuronal apoptosis were investigated in mice with TBI by controlled cortical impingement.
View Article and Find Full Text PDFPremenopausal bilateral oophorectomy and Alzheimer's disease imaging biomarkers later in life.
Alzheimers Dement
December 2024
Department of Epidemiology and Prevention, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.
Introduction: Premenopausal bilateral oophorectomy (PBO) before the age of 46 years is associated with an increased risk of dementia. We investigated the long-term effects of PBO performed before age 50 years on amyloid beta (Aβ), tau, and neurodegeneration imaging biomarkers of Alzheimer's disease (AD).
Methods: Mayo Clinic Cohort Study of Oophorectomy and Aging-2 participants were divided into early PBO (< 46 years; n = 61), and late PBO (46-49 years; n = 51) groups and were compared to referent women who did not undergo PBO (n = 119).
pTau pathology in the retina of TAU58 mice: association with ganglion cell degeneration and implications on seeding and propagation of pTau from human brain lysates.
Acta Neuropathol Commun
December 2024
Laboratory of Neuropathology, Department of Imaging and Pathology, Leuven Brain Institute, KU Leuven, Leuven, Belgium.
The accumulation of abnormal phosphorylated Tau protein (pTau) in neurons of the brain is a pathological hallmark of Alzheimer's disease (AD). PTau pathology also occurs in the retina of AD cases. Accordingly, questions arise whether retinal pTau can act as a potential seed for inducing cerebral pTau pathology and whether retinal pTau pathology causes degeneration of retinal neurons.
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