Korea is becoming an aged society at an alarmingly fast rate, which suggests that dementia care may become a major public health problem in Korea. At this point in time, the new policy of national responsibility for dementia care is a well-timed strategy, but it should be assessed based on a careful consideration of several aspects. We must promote a model of dementia care in which all members of society jointly participate. We need to improve the volunteer system in dementia care, and to make various cultural spaces for patients suffering from dementia and their family members. We need to balance financial resources and benefits in cost-reduction plans for dementia treatment. We should implement a careful quality control system for dementia care and educational programs for public dementia care hospitals and nationwide regional dementia centers. These care systems should also incorporate a health policy aiming at primary prevention to reduce the prevalence of dementia in the future. Improving the new policy of national responsibility for dementia care using detailed analyses and systematic approaches will lead to a successful dementia welfare policy.
Dementia ; Health Policy ; Humans ; Korea ; Prevalence ; Primary Prevention ; Public Health ; Quality Control ; Volunteers

No abstract available.
Air Pollution ; Dementia

Korea is becoming an aged society at an alarmingly fast rate, which suggests that dementia care may become a major public health problem in Korea. At this point in time, the new policy of national responsibility for dementia care is a well-timed strategy, but it should be assessed based on a careful consideration of several aspects. We must promote a model of dementia care in which all members of society jointly participate. We need to improve the volunteer system in dementia care, and to make various cultural spaces for patients suffering from dementia and their family members. We need to balance financial resources and benefits in cost-reduction plans for dementia treatment. We should implement a careful quality control system for dementia care and educational programs for public dementia care hospitals and nationwide regional dementia centers. These care systems should also incorporate a health policy aiming at primary prevention to reduce the prevalence of dementia in the future. Improving the new policy of national responsibility for dementia care using detailed analyses and systematic approaches will lead to a successful dementia welfare policy.

Cytotoxic lesions of the corpus callosum (CLOCC) are secondary lesions on corpus callosum caused by cytokinopathy of callosal neurons and microglia. Fever, headache, and digestive disturbances are common symptoms. Reversible and hyperintense signals on fluid‐attenuated inversion recovery imaging, diffusion‐weighted imaging (DWI) and decreased apparent diffusion coefficient are typical features of magnetic resonance imaging. Herein, we report a rare case of CLOCC caused by COVID19 vaccination (BNT162b) and discharged without no neurologic symptoms due to prompt treatment.

BACKGROUND AND PURPOSE: Amyloid beta (Aβ) is the main component of amyloid plaques, which are deposited in the brains of patients with Alzheimer's disease (AD). Biochemical and animal studies support the central role of Aβ in AD pathogenesis. Despite several investigations focused on the pathogenic mechanisms of Aβ, it is still unclear how Aβ accumulates in the central nervous system and subsequently initiates the disease at the cellular level. In this study, we investigated the pathogenic mechanisms of Aβ using proteomics and antibody microarrays. METHODS: To evaluate the effect of Aβ on neural stem cells (NSCs), we treated primary cultured cortical NSCs with several doses of Aβ for 48 h. A 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay, trypan blue staining, and bromodeoxyuridine cell proliferation assay were performed. We detected several intracellular proteins that may be associated with Aβ by proteomics and Western blotting analysis. RESULTS: Various viability tests showed that Aβ decreased NSCs viability and cell proliferation in a concentration-dependent manner. Aβ treatment significantly decreased lactate dehydrogenase B, high-mobility group box 1, aldolase C, Ezrin, and survival signals including phosphorylated phosphoinositide 3-kinase, Akt, and glycogen synthase kinase-3β. CONCLUSIONS: These results suggest that several factors determined by proteomics and Western blot hold the clue to Aβ pathogenesis. Further studies are required to investigate the role of these factors.
Alzheimer Disease ; Amyloid* ; Animals ; Blotting, Western ; Brain ; Bromodeoxyuridine ; Cell Proliferation ; Central Nervous System ; Fructose-Bisphosphate Aldolase ; Glycogen Synthase ; Humans ; L-Lactate Dehydrogenase ; Neural Stem Cells* ; Plaque, Amyloid ; Proteomics ; Trypan Blue

Background: and purpose: The anti-aging standard forest healing program (ASFHP), which uses forest therapy, was reported to be effective in improving psychological, physical, and cognitive functions. However, there are several challenges to directly visiting the forest. This study aimed to investigate the impact of multi-session ASFHP with forest visit on the mental and physical health of the older people with visits to forest facilities and compared them with those of the same program conducted indoors. Methods: Individuals aged over 70 years with concerns about cognitive decline were recruited at dementia relief centers and divided into control and experimental groups. A total of 33 people were administered ASFHP under the supervision of a forest therapy instructor. The control group stayed indoors, while the experimental group visited a forest healing center and repeated the program 20 weeks. Results: The multiple-session ASFHP positively affected cognitive impairment screening test (CIST) total scores (p=0.002), memory (p=0.014), Korean version of the Repeatable Battery for the Assessment of Neuropsychological Status total scores (p<0.001), immediate recall (p=0.001), visuospatial/construction (p<0.001), language (p<0.001), forest healing standard questionnaire total scores (p=0.002), and cognitive function (p=0.019), regardless of location. The forest visits during the ASFHP showed positive effects on orientation (p=0.035), delayed recall (p=0.042), emotional stability (p=0.032), physical activity (p=0.005), and health (p=0.022). The CIST scores of the memory domain were the strongest indicator of the multiple-session ASFHP effects. Conclusions The 20-week multi-session ASFHP with forest visit showed effects on cognitive improvement and physical and emotional stability compared to indoor education.

BACKGROUND AND PURPOSE: Neurogenesis in the adult brain is important for memory and learning, and the alterations in neural stem cells (NSCs) may be an important aspect of Alzheimer's disease (AD) pathogenesis. The phosphatidylinositol 3-kinase (PI3K) pathway has been suggested to have an important role in neuronal cell survival and is highly involved in adult neurogenesis. Candesartan is an angiotensin II receptor antagonist used for the treatment of hypertension and several studies have reported that it also has some neuroprotective effects. We investigated whether candesartan could restore the amyloid-β(25–35) (Aβ₂₅₋₃₅) oligomer-inhibited proliferation of NSCs by focusing on the PI3K pathway. METHODS: To evaluate the effects of candesartan on the Aβ₂₅₋₃₅ oligomer-inhibited proliferation of NSCs, the NSCs were treated with several concentrations of candesartan and/or Aβ₂₅₋₃₅ oligomers, and MTT assay and trypan blue staining were performed. To evaluate the effect of candesartan on the Aβ-inhibited proliferation of NSCs, we performed a bromodeoxyuridine (BrdU) labeling assay. The levels of p85α PI3K, phosphorylated Akt (pAkt) (Ser473), phosphorylated glycogen sinthase kinase-3β (pGSK-3β) (Ser9), and heat shock transcription factor-1 (HSTF-1) were analyzed by Western blotting. RESULTS: The BrdU assays demonstrated that NSC proliferation decreased with Aβ25-35 oligomer treatment; however, a combined treatment with candesartan restored it. Western blotting displayed that candesartan treatment increased the expression levels of p85α PI3K, pAkt (Ser473), pGSK-3β (Ser9), and HSTF. The NSCs were pretreated with a PI3K inhibitor, LY294002; the effects of candesartan on the proliferation of NSCs inhibited by Aβ₂₅₋₃₅ oligomers were almost completely blocked. CONCLUSIONS: Together, these results suggest that candesartan restores the Aβ₂₅₋₃₅ oligomer-inhibited proliferation of NSCs by activating the PI3K pathway.
Adult ; Alzheimer Disease ; Amyloid* ; Blotting, Western ; Brain ; Bromodeoxyuridine ; Cell Survival ; Glycogen ; Hot Temperature ; Humans ; Hypertension ; Learning ; Memory ; Neural Stem Cells* ; Neurogenesis ; Neurons ; Neuroprotective Agents ; Phosphatidylinositol 3-Kinase* ; Phosphatidylinositols* ; Receptors, Angiotensin ; Shock ; Trypan Blue

No abstract available.
Paragonimiasis ; Paragonimus westermani ; Stroke

BACKGROUND: Frontotemporal dementia (FTD) with motor neuron disease (MND) is a syndrome of progressive changes in behavior, language, muscle weakness and atrophy due to loss of function of neurons in the frontal and temporal lobes and in motor neurons. Etiology and pathogenesis of FTD with MND are still uncertain. CASE REPORT: A 71-year-old man presented with a 2-year history of progressive muscle weakness and cognitive deficits. We diagnosed this patient as FTD with MND by neurological examination, electromyography, brain imaging and neuro-psychological evaluation. We also confirmed antiphospholipid syndrome (APS) in this patient as a way to rule out secondary causes of MND. CONCLUSIONS: This was a very rare case of FTD with MND in APS. We should focus study on the possible role of autoimmune pathogenesis in FTD with MND.
Aged ; Antiphospholipid Syndrome* ; Atrophy ; Cognition Disorders ; Electromyography ; Frontotemporal Dementia* ; Humans ; Motor Neuron Disease* ; Motor Neurons* ; Muscle Weakness ; Neuroimaging ; Neurologic Examination ; Neurons ; Temporal Lobe

BACKGROUND AND PURPOSE: Alzheimer's disease (AD) is the most common form of dementia which typically manifests as loss of memory and cognitive functions. Currently, available treatments for AD provide only symptomatic improvement and the benefit is minimal. Stem cell therapy (SCT) has been considered a promising treatment option for AD. We investigated the caregiver's perception about implementation of SCT in their AD patients, and determined the factors related to SCT. METHODS: A total of 100 caregivers, who cared for their AD patients, were interviewed at two hospitals. Structured open and closed questions about SCT for AD were asked by trained interviewers using the conventional in-person method. In addition, 60 dementia-related physicians were randomly interviewed via an e-mail questionnaire. RESULTS: Of the 100 subjects, 61 caregivers replied that they wanted their AD patients to receive SCT. Approximately 50% of the caregivers expected high improvement in cognitive function, behavioral and psychological symptoms, and activities of daily living, and physical improvements among their AD patients. However, physicians had much lower expectations of improvements in the above parameters. Multi-variate analysis revealed that female gender [odds ratio (OR): 3.747, 95% confidence interval (CI): 1.425–9.851] and familiarity with stem cells (OR: 3.873, 95% CI: 1.290–11.622) were independently associated with caregivers' desire that their AD patients should undergo SCT. The major source of information on SCT was television (76.7%), and the most reliable source of information on SCT was physicians (83.6%). CONCLUSIONS: In this study, many caregivers of AD patients fantasized and overestimated the need for SCT in comparison with physicians' expectation. Therefore, it is necessary for physicians to develop strategies for educating caregivers about the appropriate risks and benefits of SCT.
Activities of Daily Living ; Alzheimer Disease ; Caregivers ; Cognition ; Dementia ; Electronic Mail ; Female ; Humans ; Memory ; Methods ; Recognition (Psychology) ; Risk Assessment ; Stem Cells* ; Television