Background And Purpose: The Brain Atrophy and Lesion Index combines several common, aging-related structural brain changes and has been validated for high-field MR imaging. In this study, we evaluated measurement properties of the Brain Atrophy and Lesion Index by use of T1WI and T2WI at 1.5T and 3T MR imaging to comprehensively assess the usefulness of the lower field-strength testing.
Materials And Methods: Data were obtained from the Alzheimer's Disease Neuroimaging Initiative. Images of subjects (n = 127) who had T1WI and T2WI at both 3T and 1.5T on the same day were evaluated, applying the Brain Atrophy and Lesion Index rating. Criterion and construct validity and interrater agreement were tested for each field strength and image type.
Results: Regarding reliability, the intraclass correlation coefficients for the Brain Atrophy and Lesion Index score were consistently high (>0.81) across image type and field strength. Regarding construct validity, the Brain Atrophy and Lesion Index score differed among diagnostic groups, being lowest in people without cognitive impairment and highest in those with Alzheimer disease (F > 5.14; P < .007). Brain Atrophy and Lesion Index scores correlated with age (r > 0.37, P < .001) and cognitive performance (r > 0.38, P < .001) and were associated with positive amyloid-β test (F > 3.96, P < .050). The T1WI and T2WI Brain Atrophy and Lesion Index scores were correlated (r > 0.93, P < .001), with the T2WI scores slightly greater than the T1WI scores (F > 4.25, P < .041). Regarding criterion validation of the 1.5T images, the 1.5T scores were highly correlated with the 3T Brain Atrophy and Lesion Index scores (r > 0.93, P < .001).
Conclusions: The higher field and T2WI more sensitively detect subtle changes in the deep white matter and perivascular spaces in particular. Even so, 1.5T Brain Atrophy and Lesion Index scores are similar to those obtained by use of 3T images. The Brain Atrophy and Lesion Index may have use in quantifying the impact of dementia on brain structures.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7964740 | PMC |
| http://dx.doi.org/10.3174/ajnr.A3709 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Dysregulation of the Kynurenine Pathway in Relapsing Remitting Multiple Sclerosis and Its Correlations With Progressive Neurodegeneration.
Neurol Neuroimmunol Neuroinflamm
March 2025
Macquarie Medical School, Faculty of Medicine, Health and Human Sciences, Macquarie University, Sydney.
Background And Objectives: Despite the absence of acute lesion activity in multiple sclerosis (MS), chronic neurodegeneration continues to progress, and a potential underlying mechanism could be the kynurenine pathway (KP). Prolonged activation of the KP from chronic inflammation is known to exacerbate the progression of neurodegenerative diseases through the production of neurotoxic metabolites. Among the 8 KP metabolites, six of them, namely kynurenine (KYN), 3-hydroxylkynurenine (3HK), anthranilic acid (AA), kynurenic acid (KYNA), and quinolinic acid (QUIN), have been associated with neurodegeneration.
View Article and Find Full Text PDFIntroduction: Diagnosing dementia remains challenging in low-income settings due to limited diagnostic options and the absence of definitive biomarkers. The use of brain MRI in the diagnosis of dementia is infrequent in Uganda, and even when it is used, subtle findings like mild regional atrophy are often overlooked, despite being crucial for imaging diagnosis.
Objective: The purpose of this study was to explore the perceptions and practices of imaging personnel and physicians regarding the use of brain MRI as a diagnostic approach for dementia in Uganda.
Neural deterioration and compensation in visual short-term memory among individuals with amnestic mild cognitive impairment.
Alzheimers Dement
January 2025
Guangdong Provincial Key Laboratory of Brain Function and Disease, Center for Brain and Mental Well-Being, Department of Psychology, Sun Yat-sen University, Guangzhou, China.
Introduction: Visual short-term memory (VSTM) is a critical indicator of Alzheimer's disease (AD), but whether its neural substrates could adapt to early disease progression and contribute to cognitive resilience in amnestic mild cognitive impairment (aMCI) has been unclear.
Methods: Fifty-five aMCI patients and 68 normal controls (NC) performed a change-detection task and underwent multimodal neuroimaging scanning.
Results: Among the atrophic brain regions in aMCI, VSTM performance correlated with the volume of the right prefrontal cortex (PFC) but not the medial temporal lobe (MTL), and this correlation was mainly present in patients with greater MTL atrophy.
Delayed Progression of Ataxia with a Static Cerebellar Lesion- Consider SCA27B.
Cerebellum
January 2025
Department of Neurology, Donders Institute for Brain, Cognition & Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
Repeat expansions in the fibroblast growth factor 14 gene (FGF14), associated with spinocerebellar ataxia type 27B (SCA27B), have emerged as a prevalent cause of previously unexplained late-onset cerebellar ataxia. Here, we present a patient with residual symptom of gait ataxia after complicated meningioma surgery, who presented with progressive symptoms of oculomotor disturbances, speech difficulties, vertigo and worsening of gait imbalance, twelve years post-resection. Neuroimaging revealed a surgical resection cavity in the dorsolateral side of the left cerebellar hemisphere, accompanied by gliosis in left cerebellar hemisphere extending into the vermis, extensive non-specific supratentorial periventricular white matter abnormalities, and mild atrophy of the cerebellar vermis.
View Article and Find Full Text PDFNeural Stem/Progenitor Cell Therapy in Patients and Animals with Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-analysis.
Mol Neurobiol
January 2025
Hebei Medical University-Galway University Stem Cell Research Center, Hebei Medical University, Shijiazhuang, Hebei Province, 050017, China.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative malady that causes progressive degeneration and loss of motor neuron function in the brain and spinal cord, eventually resulting in muscular atrophy, paralysis, and death. Neural stem/progenitor cell (NSPC) transplantation can improve bodily function in animals and delay disease progression in patients with ALS. This paper summarizes and analyzes the efficacy and safety of neural stem/progenitor cell (NSPC) transplantation as a treatment for ALS, aiming to improve function and delay disease progression in patients.
View Article and Find Full Text PDFWant 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!