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Structural brain changes in aging are known to occur even in the absence of dementia, but the magnitudes and regions involved vary between studies. To further characterize these changes, we analyzed paired MRI images acquired with identical protocols and scanner over a median 5.8-year interval. The normal study group comprised 78 elders (25M 53F, baseline age range 70-78 years) who underwent an annual standardized expert assessment of cognition and health and who maintained normal cognition for the duration of the study. We found a longitudinal grey matter (GM) loss rate of 2.56 ± 0.07 ml/year (0.20 ± 0.04%/year) and a cerebrospinal fluid (CSF) expansion rate of 2.97 ± 0.07 ml/year (0.22 ± 0.04%/year). Hippocampal volume loss rate was higher than the GM and CSF global rates, 0.0114 ± 0.0004 ml/year (0.49 ± 0.04%/year). Regions of greatest GM loss were posterior inferior frontal lobe, medial parietal lobe and dorsal cerebellum. Rates of GM loss and CSF expansion were on the low end of the range of other published values, perhaps due to the relatively good health of the elder volunteers in this study. An additional smaller group of 6 subjects diagnosed with MCI at baseline were followed as well, and comparisons were made with the normal group in terms of both global and regional GM loss and CSF expansion rates. An increased rate of GM loss was found in the hippocampus bilaterally for the MCI group.
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http://dx.doi.org/10.3934/Neuroscience.2020009 | DOI Listing |
Front Neurol
August 2025
Department of Neurology, West China Hospital of Sichuan University, Chengdu, China.
Familial frontotemporal dementia (FTD) is a genetically heterogeneous disease with various clinical manifestations, making it difficult to diagnose. There are three main gene mutations in familial FTD: repeat expansion in chromosome 9 open reading frame 72 (), microtubule-associated protein tau (), and progranulin (). These mutations can produce corresponding changes in fluid biomarkers years before symptoms appear.
View Article and Find Full Text PDFInt J Mol Sci
August 2025
Puls Med Association, 051885 Bucharest, Romania.
Amyotrophic lateral sclerosis (ALS) is still a heterogeneous neurodegenerative disorder that can be identified clinically and biologically, without a strong set of biomarkers that can adequately measure its fast rate of progression and molecular heterogeneity. In this review, we intend to consolidate the most relevant and timely advances in ALS biomarker discovery, in order to begin to bring molecular, imaging, genetic, and digital areas together for potential integration into a precision medicine approach to ALS. Our goal is to begin to display how several biomarkers in development (e.
View Article and Find Full Text PDFNeurology
September 2025
Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD.
This case of encephalomyelitis in a previously healthy 21-year-old man who developed opsoclonus-myoclonus demonstrates the diagnostic utility of clinically validated metagenomic next-generation sequencing (mNGS), followed by appropriate confirmation, in complex cases of encephalitis. In this patient, an extensive diagnostic workup was negative for infectious, inflammatory, demyelinating, autoimmune, and paraneoplastic etiologies. However, clinically validated mNGS of the CSF identified human pegivirus (HPgV) as a potential causative agent.
View Article and Find Full Text PDFCell
August 2025
Goizueta Brain Health Institute Center for Neurodegenerative Diseases, Emory University, Atlanta, GA 30322, USA; Department of Neurology, Emory University, Atlanta, GA 30322, USA; Department of Pathology, Emory University, Atlanta, GA 30322, USA. Electronic address:
C9orf72-associated amyotrophic lateral sclerosis (c9ALS) is caused by an intronic GC repeat expansion that leads to toxic RNA transcripts and dipeptide repeat proteins (DPRs). A clinical trial using the antisense oligonucleotide (ASO) BIIB078 to target these transcripts was discontinued after failing to provide clinical benefit. Here, we determine the extent of target engagement in the central nervous system (CNS) and elucidate pharmacodynamic cerebrospinal fluid (CSF) biomarkers following treatment.
View Article and Find Full Text PDFUltrasound Obstet Gynecol
April 2025
Maternal Fetal Care Center, Division of Fetal Medicine and Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Aqueductal stenosis is a specific type of non- communicating hydrocephalus, which is characterized by narrowing or constriction of the cerebral aqueduct, also known as the aqueduct of Sylvius. Due to the blockage, the flow of cerebrospinal fluid (CSF) through the aqueduct becomes restricted or obstructed, leading to an abnormal accumulation of CSF within the ventricles and increased intracranial pressure. Progressive expansion of the ventricles leads to increasing cerebral mantle compression during fetal brain development, which can lead to irreversible damage with deleterious consequences.
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