OBJECTIVES: A retrospective study on the efficacy of melatonin in treatment of sleep and cognitive disorders of Alzheimer's disease was conducted. METHODS: Fourteen patients (8 females, 6 males), mean +/- S.D. age 72 +/- 9 years were included. All patients received 9 mg gelatin melatonin capsules p.o. daily at bedtime for 22 to 35 months. Overall quality of sleep was assessed from sleep logs filled in by the patients or their caretakers. Neuropsychological evaluation was performed by Functional Assessment Tool For Alzheimer's Disease (FAST), Mini-Mental, Alzheimer's Disease Assessment Scale (ADAS), and Mattis' and Blessed's scales. At diagnosis, all patients had cognitive and neuroimaging alterations (cortical and bitemporal atrophy) compatible with different evolutionary stages of the disease. RESULTS: At the time of assessment, a significant improvement of sleep quality was found in all cases examined. There were no significant differences between initial and present evaluation in scores of FAST, Mini-Mental, and ADAS, and of Mattis' and Blessed's scales. Clinically, the patients exhibited lack of progression of the cognitive and behavioral signs of the disease during the time they received melatonin. Sundowning was no longer detectable in 12 patients and persisted, although attenuated, in 2 patients. CONCLUSION. The results suggest that melatonin can be useful for treatment of Alzheimer's disease.
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Ann Neurol
January 2025
Research Unit of Neurology, Neurophysiology and Neurobiology, Department of Medicine and Surgery, Università Campus Bio-Medico di Roma, Rome, Italy.
Objective: Despite diagnostic criteria refinements, Parkinson's disease (PD) clinical diagnosis still suffers from a not satisfying accuracy, with the post-mortem examination as the gold standard for diagnosis. Seminal clinicopathological series highlighted that a relevant number of patients alive-diagnosed with idiopathic PD have an alternative post-mortem diagnosis. We evaluated the diagnostic accuracy of PD comparing the in-vivo clinical diagnosis with the post-mortem diagnosis performed through the pathological examination in 2 groups.
View Article and Find Full Text PDFJ Imaging Inform Med
January 2025
Faculty of Mathematics and Information Science, Warsaw University of Technology, Warsaw, Poland.
Analysis of the symmetry of the brain hemispheres at the level of individual structures and dominant tissue features has been the subject of research for many years in the context of improving the effectiveness of imaging methods for the diagnosis of brain tumor, stroke, and Alzheimer's disease, among others. One useful approach is to reliably determine the midline of the brain, which allows comparative analysis of the hemispheres and uncovers information on symmetry/asymmetry in the relevant planes of, for example, CT scans. Therefore, an effective method that is robust to various geometric deformations, artifacts, varying noise characteristics, and natural anatomical variability is sought.
View Article and Find Full Text PDFBrain Inform
January 2025
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Cognitive resilience (CR) describes the phenomenon of individuals evading cognitive decline despite prominent Alzheimer's disease neuropathology. Operationalization and measurement of this latent construct is non-trivial as it cannot be directly observed. The residual approach has been widely applied to estimate CR, where the degree of resilience is estimated through a linear model's residuals.
View Article and Find Full Text PDFEur Radiol
January 2025
Chulalongkorn University Biomedical Imaging Group, Department of Radiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Commun Med (Lond)
January 2025
Rare Disease Translational Center, The Jackson Laboratory, Bar Harbor, ME, USA.
Background: Multiple Sulfatase Deficiency (MSD) is a rare inherited lysosomal storage disorder characterized by loss of function mutations in the SUMF1 gene that manifests as a severe pediatric neurological disease. There are no available targeted therapies for MSD.
Methods: We engineered a viral vector (AAV9/SUMF1) to deliver working copies of the SUMF1 gene and tested the vector in Sumf1 knock out mice that generally display a median lifespan of 10 days.
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