Background: White matter hyperintensities (WMHs) and regional brain lobe atrophy coexist in the brain of patients with Alzheimer's disease (AD), but the association between them in patients with AD still lacks comprehensive investigation and solid imaging data support.
Objective: We explored whether WMHs can promote the pathological process of AD by aggravating atrophy in specific brain regions and tried to explain the regional specificity of these relationships.
Methods: A sample of 240 adults including 180 normal controls (NCs) and 80 cases with AD were drawn from the ADNI database. T1-weighted magnetic resonance imaging (MRI) and T2-weighted fluid-attenuated MRI of the participants were downloaded and were analyzed using AccuBrain to generate the quantitative ratio of WMHs (WMHr, WMH volumes corrected by intracranial volume) and regional brain atrophy. We also divided WMHr into periventricular WMHr (PVWMHr) and deep WMHr (DWMHr) for the purpose of this study. The Cholinergic Pathways Hyperintensities Scale (CHIPS) scores were conducted by two evaluators. Independent -test, Mann-Whitney test, or χ test were used to compare the demographic characteristics, and Spearman correlation coefficient values were used to determine the association between WMHs and different regions of brain atrophy.
Results: Positive association between WMHr and quantitative medial temporal lobe atrophy (QMTA) ( = 0.281, = 0.011), temporal lobe atrophy ( = 0.285, = 0.011), and insular atrophy ( = 0.406, < 0.001) was found in the AD group before Bonferroni correction. PVWMHr contributed to these correlations. By separately analyzing the relationship between PVWMHr and brain atrophy, we found that there were still positive correlations after correction in QMTA ( = 0.325, = 0.003), temporal lobe atrophy ( = 0.298, = 0.007), and insular atrophy ( = 0.429, < 0.001) in AD group.
Conclusion: WMH severity tends to be associated with regional brain atrophy in patients with AD, especially with medial temporal lobe, temporal lobe, and insular lobe atrophy. PVWMHs were devoted to these correlations.
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http://dx.doi.org/10.3389/fnhum.2022.760360 | DOI Listing |
Brain Sci
November 2024
Clinical Neuroanatomy, Department of Neurology, University Hospital Ulm, 89081 Ulm, Germany.
Creativity and the production of artwork can have an impact on the course and treatment of comorbid severe mental illness and neurodegeneration. We report on a 70-year-old male patient with highly original artistic behavior, who suffered from lifelong recurrent major depression and subsequently developed symptoms of progressive bulbar palsy (PBP). In the context of a systematic literature review, we detail the patient's personal and artistic biographies and portray artwork from his artistic portfolio together with his disease history, clinical examination, psychopathological and neuropsychological evaluations, blood and cerebrospinal fluid analyses, neuroimaging, neurophysiological testing, and psychotherapeutic treatment.
View Article and Find Full Text PDFIntroduction: Hippocampal hyperactivity is a hallmark of prodromal Alzheimer's disease (AD) that predicts progression in patients with amnestic mild cognitive impairment (aMCI). AGB101 is an extended-release formulation of levetiracetam in the dose range previously demonstrated to normalize hippocampal activity and improve cognitive performance in aMCI. The HOPE4MCI study was a 78-week trial to assess the progression of MCI due to AD.
View Article and Find Full Text PDFAgeing Res Rev
December 2024
Division of Psychiatry, University College London, Maple House, 149 Tottenham Court Road, London W1T 7NF, UK; North London NHS Foundation Trust, London, 4 St Pancras Way, London NW1 0PE, UK. Electronic address:
Background And Objective: People with adult-onset hearing loss (AoHL) are at increased dementia risk. In this study, we explore potential aetiological mechanisms by synthesising the evidence on the association between AoHL and neuropathological, cerebrospinal fluid (CSF), blood and imaging biomarkers of dementia.
Methods: We systematically searched electronic databases from inception to 30 April 2024 for cross-sectional and longitudinal studies, including quantitative data on the association between AoHL and dementia biomarkers.
Asia Ocean J Nucl Med Biol
January 2025
Department of Radiology, Fujita Health University School of Medicine, Aichi, Japan.
Objectives: Sudden death in multiple system atrophy (MSA) is caused by decreased serotonergic innervation, but there is no routine test method for this decrease. In addition to dopamine transporters, iodine-123-labelled N-(3-fluoropropyl)-2β-carbomethoxy-3β-(4-iodophenyl) nortropane (I-FP-CIT) binds serotonin transporters (SERTs). We noted a binding potential to quantify the total quantity of I-FP-CIT binding to its receptors.
View Article and Find Full Text PDFAppl Neuropsychol Adult
December 2024
Department of Clinical Psychology, William James College, Newton, MA, USA.
Objective: Little is known about the relative contribution of frontal and anterior temporal lobes in semantic knowledge of social norms in frontotemporal dementia (FTD). Therefore, this study examined performance of FTD patients with either frontal (F-FTD, left temporal (LT-FTD) or bitemporal lobe atrophy (BT-FTD) on the Social Norms Questionnaire (SNQ) and explored what accounts for the variance in the SNQ-break norm subscale (i.e.
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