Background: Prodromal stage of Lewy Body Dementia (LBD) is characterized by a set of symptoms that do not yet meet the criteria for dementia. These symptoms are caused by changes in the brain that have not yet reached the threshold for triggering the disease in its complete form. Identifying the prodromal stage of neurodegenerative diseases is crucial for early treatment and prevention of progression to a clinical stage. This study aimed to determine the clinical profile in the prodromal stage of LBD in a population of Argentina.
Method: Over six months, we recruited subjects with dementia and a control group of individuals without neurocognitive disorder (NC). All participants underwent a comprehensive medical history, neuropsychological tests, and neuroimaging. Dementia patients were divided into two groups: Group 1 consisted of patients with probable DLB according to the consensus criteria of McKeith et al. 2017. Group 2 consisted of patients with Major Neurocognitive Disorder due to Alzheimer's Disease (AD) according to DSM V criteria. To detect the presence of early clinical signs, we interviewed family members of patients based on central and supportive clinical signs according to Consortium-DLB 2017 that may have been present up to 20 years before the dementia diagnosis.
Result: The study included 212 participants; 56 were classified as NC, 72 in Group 1, and 84 in Group 2. No significant differences were observed in sociodemographic factors. Notably, LBD patients exhibited a higher frequency of REM sleep behavior disorder (12.5%), visual hallucinations (9.7%), and syncope (9.7%) compared to the other groups, with statistical significance (p<0.01). Other variables did not show significant differences.
Conclusion: In this population with LBD, visual hallucinations, syncope, and REM sleep behavior disorder may occur more than 20 years before the onset of dementia and constitute signs of the prodromal stage. Encouraging the search for these symptoms is essential since they are not frequently questioned in patients with mild cognitive complaints.
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http://dx.doi.org/10.1002/alz.086436 | DOI Listing |
BMC Neurol
January 2025
Department of Neurology, The First Affiliated Hospital of Zhengzhou University, 1 East Jianshe Road, Zhengzhou, China.
Background: Awareness of the characteristics of glial fibrillary acidic protein autoantibody (GFAP-IgG) associated myelitis facilitates early diagnosis and treatment. We explored features in GFAP-IgG myelitis and compared them with those in myelitis associated with aquaporin-4 IgG (AQP4-IgG) and myelin oligodendrocyte glycoprotein IgG (MOG-IgG).
Methods: We retrospectively reviewed data from patients with GFAP-IgG myelitis at the First Affiliated Hospital of Zhengzhou University and Henan Children's Hospital from May 2018 to May 2023.
Alzheimers Dement
December 2024
Washington University School of Medicine, St. Louis, MO, USA.
Background: P-tau217 has emerged as a compelling alternative to long-established p-tau181 to accurately measure tau modifications in biofluids in response to brain Abeta and tau deposition in Alzheimer's disease (AD). Understanding the specificity and significance of p-tau217 changes over AD stages is critical to interpret its potential response to treatments against Abeta and tau aggregation.
Methods: We measured p-tau217 phosphorylation by mass spectrometry.
Alzheimers Dement
December 2024
Centre for Healthy Brain Ageing (CHeBA), University of New South Wales, UNSW Sydney, NSW, Australia.
Background: Subjective Cognitive Complaints (SCCs) can often precede mild cognitive impairment and dementia longitudinally. While increasingly considered an early prodromal stage of dementia, SCCs can also be a symptom of depression. Previous research found that SCCs in the absence of cognitive impairment, controlling for symptoms of depression, were moderately heritable and genetically associated with memory.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neurologia, Azienda Ospedaliero Universitaria di Modena, Modena, Italy.
Background: Recent evidence suggests that unawareness in Alzheimer's disease (AD) continuum can be explained by a failure of the connections between brain regions involved in accessing and monitoring self and other information. It has been demonstrated that AD patients with anosognosia have reduced network connectivity in the default mode network (DMN); in addition, stronger connectivity of bilateral anterior cingulate cortex (ACC) was showed to be associated with anosognosia in prodromal AD suggesting a possible role of this region in mechanisms of "adaptation" to anosognosia early in the disease. Therefore, we hypothesized that anosognosia in AD could be associated with an imbalance between the activity of the DMN and the salience network (SN) detectable using resting state functional magnetic resonance imaging (fMRI).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Hospital Italiano de Buenos Aires, Buenos aires, Argentina.
Background: Prodromal stage of Lewy Body Dementia (LBD) is characterized by a set of symptoms that do not yet meet the criteria for dementia. These symptoms are caused by changes in the brain that have not yet reached the threshold for triggering the disease in its complete form. Identifying the prodromal stage of neurodegenerative diseases is crucial for early treatment and prevention of progression to a clinical stage.
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