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• The mobile health intervention is effective for self-efficacy in people with PD. • In addition, the intervention is effective for non-motor symptoms in people with PD. • The IMB model could be helpful in improving self-management in individuals with PD. To evaluate the effects of a mobile health intervention for self-management on self-efficacy, motor and non-motor symptoms, self-management, and quality of life in people with Parkinson's disease. A randomized controlled design was used. The participants were randomly assigned to an intervention or a control group. The intervention group (n = 20) received mobile health intervention comprising mobile applications, smartwatches, smartphone-based short text messages and information, and telephone counselling; whereas the control group (n = 23) received short text messages and telephone counselling for 16 weeks. After 16 weeks, self-efficacy and non-motor symptom scores in the intervention group significantly improved compared to those in the control group. However, no significant differences were observed in the motor symptoms, self-management, and quality of life between the groups. The mobile health intervention for self-management is effective for self-efficacy and non-motor symptoms in people with Parkinson's disease. [ABSTRACT FROM AUTHOR]

Background: Around 15% to 20% of patients with clinically probable Alzheimer disease have been found to have no significant Alzheimer pathology on amyloid positron emission tomography. A previous study showed that conversion to dementia from amyloid-negative mild cognitive impairment (MCI) was observed in up to 11% of patients, drawing attention to this condition.Object: We gathered the detailed neuropsychological and neuroimaging data of this population to elucidate factors for conversion to dementia from amyloid-negative amnestic MCI.Methods: This study was a single-institutional, retrospective cohort study of amyloid-negative MCI patients over age 50 with at least 36 months of follow-up. All subjects underwent detailed neuropsychological testing, 3 tesla brain magnetic resonance imaging), and fluorine-18(18F)-florbetaben amyloid positron emission tomography scans.Results: During the follow-up period, 39 of 107 (36.4%) patients converted to dementia from amnestic MCI. The converter group had more severe impairment in all visual memory tasks. The volumetric analysis revealed that the converter group had significantly reduced total hippocampal volume on the right side, gray matter volume in the right lateral temporal, lingual gyri, and occipital pole.Conclusion: Our study showed that reduced gray matter volume related to visual memory processing may predict clinical progression in this amyloid-negative MCI population. [ABSTRACT FROM AUTHOR]

Amyloid (Aβ) and tau proteins are pathologic hallmarks of Alzheimer disease (AD). It is well known that there is spatial disparity between Aβ and tau protein deposition but, crossed hemispheric accumulation of these 2 proteins has not been reported. Here we report the case of a 76-year-old woman with typical AD who underwent amyloid positron emission tomography (PET) ([ 18 F]-florbetaben) and tau PET scans ([ 18 F]PI-2620), revealing crossed accumulation of Aβ and tau in the cerebral hemisphere. A neuropsychological assessment showed impairment in memory with spared activities of daily living. In the PET analysis, amyloid deposition was observed only in the left side of the cerebral hemisphere and tau only in the right side. Neuroimaging follow-up indicated that the spatial pattern of these protein accumulations had not changed. This case suggests the possibility of independent Aβ and tau pathogenic pathways in AD. [ABSTRACT FROM AUTHOR]

Background: Amyloid positron emission tomography (PET) imaging is appropriate for patients with atypical presentation, unusually rapid course and very early onset of dementia. Standardized uptake value ratios (SUVr) are used for relative quantification of 18F‐florbetaben (18F‐FBB) PET scans and cerebellar cortex can be used as reference region for quantification. Previous study showed that 18F‐FBB PET demonstrated a diffuse cortical uptake and in particular an intense uptake in the basal ganglia in familial Alzheimer’s disease with presenilin‐1(PS‐1) mutation. Method: This report describes the case of a young woman with early‐onset familial Alzheimer’s disease(EOfAD), who has atypical pattern of uptake on amyloid PET. Result: A 37‐year‐old woman with a college level educational background was brought in by her family for further evaluation of cognitive impairment, personality and behavioral changes. At age 30 years of age, the patient presented memory impairment and she had difficulty serving guests in bakery. Patient had positive family history of early onset dementia; her father, grand mother, and two sisters of grand mother. (Fig. 1 Pedigree showing autosomal dominant inheritance trait of early‐onset dementia. (nn/nn) Age at onset/age at death). She had an initial Mini‐Mental State Examination score of 22/30 (time disorientation, dyscalculia, poor delayed recall). Neuropsychological assessment showed global cerebral dysfunction and revealed dementia with psychiatric symptoms. Brain magnetic resonance imaging showed no significant abnormality. On genetic testing, homozygotes for the apolipoprotein E ε3 allele and a PS‐1 mutation (c.616G>A , p.G602S) was identified. 18F‐FBB PET revealed diffusely increased amyloid deposition including not only bilateral frontal, parietal, posterior cingulate gyrus/precuneus, anterior striatum but also bilateral cerebellar cortex. (Fig. 2 18F‐florbetaben PET, at age 37) Conclusion: This will be the first case report of EOfAD with increased bilateral cerebellar cortical uptake on 18F‐ FBB PET, we present the case to increase awareness of this unusual entity. [ABSTRACT FROM AUTHOR]

Background: Around 15–20% of patients with clinically probable Alzheimer’s disease have been found to have no significant Alzheimer’s pathology on amyloid PET. A previous study shows that conversion to dementia from amyloid‐negative mild cognitive impairment (MCI) was observed in up to 11% of patients, drawing attention to this condition. We gathered the detailed neuropsychological and neuroimaging data of this population to elucidate factors for conversion to dementia from amyloid‐negative amnestic MCI. Method: This study was a retrospective cohort study of patients over the age 50 with amyloid‐negative amnestic MCI who visited the memory clinic of Asan Medical Center with no less than a 36 months follow‐up period. All subjects underwent detailed neuropsychologic tests, three tesla brain magnetic resonance imaging (MRI) scans including 3‐dimensional T1 imaging, and fluorine‐18[F18]‐florbetaben amyloid PET scans. Result: During the 36 months of follow‐up, 39 of 107 (36.4%) patients converted to dementia from amnestic MCI. The volumetric analysis revealed that the converter group had significantly reduced total hippocampal volume on the right side, gray matter volume in the right lateral temporal, lingual gyri, and occipital pole. In terms of cerebellar gray matter (GM) volumetric analysis, reduced Crus I/II volume adjusted with total intracranial volume (TIV) and age was observed in the converter group. The converter group had also more severe impairments in all visual memory tasks. Conclusion: Our study showed that the reduced gray matter volume related to visual memory processing in the cerebrum and Significant cerebellar GM atrophy involving the bilateral Crus I/II may predict the clinical progression in this amyloid‐negative MCI population. [ABSTRACT FROM AUTHOR]

Background: Pathophysiology of cognitive decline in CAA is multifactorial, because microbleeds, white matter hyperintensities, and combined concomitant parenchymal Alzheimer’s disease (AD) pathology have been suggested to cause cognitive impairment. The mechanism by which microbleeds affect cognitive impairment is still under investigation. We aimed to investigate the mechanism of how microbleeds contribute to cognitive impairment, in association with white matter tract abnormalities or cortical thickness in CAA with significant amyloid deposition. Method: We retrospectively investigated 30 patients with probable CAA according to Boston criteria and 30 patients with Alzheimer’s disease (AD), all of whom showed severe amyloid deposition on amyloid PET (Aβ+). Age, sex, and clinical deteriorating scale were matched. Using MRI, cortical thickness and white matter tract abnormalities as fractional anisotropy (FA) were obtained. We compared cortical thickness, FA, and cognitive scores of five domains between Aβ+ CAA and Aβ+ AD. Using path analysis, we investigated the correlation between number of regional microbleeds, cortical thickness, FA, and cognitive impairments. Result: Both CAA and AD group showed similar cortical amyloid deposition in AD related regions such as precuneus, and posterior cingulate cortex suggesting that CAA in this study might have AD pathology. Patients with Aβ+ CAA presented with significantly lower FA in clusters of posterior area than patients with Aβ+ AD (FWE‐corrected p value <0.05) Importantly, total number of microbleeds were associated with decreased FA in tapetum of corpus callosum (r=‐0.429, p<0.001), which were consequently associated with visuospatial function (r=0.466, p<0.001). Cortical thickness was not significantly different between CAA and AD, and it did not mediate the association between regional microbleeds and cognition. Conclusion: This study suggests that lobar microbleeds may impact cognitive decline through the mediation of white matter tract abnormalities in CAA. [ABSTRACT FROM AUTHOR]