This paper reports the first quantitative measurements of the reflectance spectrum of the nerve fiber layer (NFL) of the retina. An arcuate defect in the NFL of two macaque monkeys was produced by photocoagulating a small spot near the optic disc. Imaging fundus reflectometry at 8 wavelengths was then used to measure the fundal reflectances in the defect and in the intact NFL. The reflectance of the NFL alone was determined by subtracting the reflectance of the bare fundus in the defect from the reflectance of the adjoining fundus with intact NFL. The reflectance data were corrected for the transmission of the ocular media with published values of the density of monkey cornea and lens. Lens absorption was measured from Purkinje images and differed little from the published values. The NFL reflectance can be characterized by a spectrum that has the same shape at all points along an arcuate region of the NFL but decreases in absolute reflectance as the thickness of the NFL decreases. The reflectance changes little between 680 and 560 nm, but rises as lambda-n from 560 to 460 nm, where n = 2.5-3.1. The data reported here begin to provide a quantitative understanding of empirically determined methods for enhancing the visibility of the NFL and have implications for retinal densitometry.
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Clin Exp Immunol
January 2025
Department of Clinical Laboratory, State key Laboratory of Complex, Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, China.
Neuro-Behçet's disease (NBD) is a more severe but rare symptom of Behçet's disease (BD), which is mainly divided into parenchymal NBD (p-NBD) involving brain stem, spinal cord, and cerebral cortex. Non-p-NBD manifests as intracranial aneurysm, cerebral venous thrombosis, peripheral nervous system injuries, and mixed parenchymal and non-parenchymal disease. P-NBD is pathologically characterized by perivasculitis presenting with cerebrospinal fluid (CSF) pleocytosis, elevated total protein, and central nervous system (CNS) infiltration of macrophages and neutrophils, which are subdivided into acute and chronic progressive stages according to relapsing-remitting courses and responses to steroids.
View Article and Find Full Text PDFTransl Psychiatry
January 2025
Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
Plasma biomarkers have great potential in the screening, diagnosis, and monitoring of Alzheimer's disease (AD). However, findings on their associations with cerebral perfusion and structural changes are inconclusive. We examined both cross-sectional and longitudinal associations between plasma biomarkers and cerebral blood flow (CBF), gray matter (GM) volume, and white matter (WM) integrity.
View Article and Find Full Text PDFHeliyon
December 2024
Department of Medicine, Faculty of Medicine and Health Sciences, and Institute of Neurosciences, University of Barcelona, Barcelona, Spain.
In early-stage Alzheimer's disease (AD) amyloid-β (Aβ) deposition can induce neuronal hyperactivity, thereby potentially triggering activity-dependent neuronal secretion of phosphorylated tau (p-tau), ensuing tau aggregation and spread. Therefore, cortical excitability is a candidate biomarker for early AD detection. Moreover, lowering neuronal excitability could potentially complement strategies to reduce Aβ and tau buildup.
View Article and Find Full Text PDFEur J Neurol
January 2025
Institut du Cerveau-Paris Brain Institute ICM, Sorbonne Université, Inserm 1127, CNRS 7225, Hôpital de la Pitié Salpêtrière Paris, Paris, France.
Objective: Spinocerebellar ataxias (SCA) are neurodegenerative diseases with widespread lesions across the central nervous system. Ataxia and spasticity are usually predominant, but patients may also present with parkinsonism. We aimed to characterize substantia nigra pars compacta (SNc) degeneration in SCA2 and 7 using neuromelanin-sensitive imaging.
View Article and Find Full Text PDFAlzheimers Res Ther
December 2024
Faculty of Health, Medicine and Life Sciences, Mental Health and Neuroscience Research Institute, Alzheimer Centre Limburg, Maastricht University, Maastricht, The Netherlands.
Background: Although separate lines of research indicated a moderating role of sex in both sleep-wake disruption and in the interindividual vulnerability to Alzheimer's disease (AD)-related processes, the quantification of sex differences in the interplay between sleep-wake dysregulation and AD pathology remains critically overlooked. Here, we examined sex-specific associations between circadian rest-activity patterns and AD-related pathophysiological processes across the adult lifespan.
Methods: Ninety-two cognitively unimpaired adults (mean age = 59.
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