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

In critically ill patients, disseminated intravascular coagulation (DIC) is a common and fatal hematological disorder. DIC is a physiological response to a variety of underlying stimuli that provoke generalized activation of the hemostatic mechanism and is common in septic patients and those with hematological or non-hematological malignant neoplasms. Bleeding is a common clinical feature, and diffuse or multiple-site mucocutaneous bleeding, such as petechia, ecchymosis and hemorrhage from gastrointestinal tract, is often seen. A 58-year-old male was recently diagnosed with intracranial hemorrhage (ICH) caused by DIC associated with sepsis. Mortality of ICH caused by DIC is very high because the underlying condition cannot be quickly treated. Awareness of the possibility of DIC developing in a critically ill patient and the need for immediate initiation of plasma or platelet replacement therapy are important. To the best of our knowledge, this is the first reported case of intracranial hemorrhage in a Korean patient with DIC associated with sepsis.
Blood Platelets ; Critical Illness ; Dacarbazine ; Disseminated Intravascular Coagulation* ; Ecchymosis ; Gastrointestinal Tract ; Hemorrhage ; Humans ; Intracranial Hemorrhages* ; Male ; Middle Aged ; Mortality ; Plasma ; Sepsis*

No abstract available.
Paragonimiasis ; Paragonimus westermani ; Stroke

Antiphospholipid syndrome may be associated with various neurologic conditions. Pseudotumor cerebri is a rare complication of the disease and is often attributed to venous thrombosis. We report a 18-year-old woman with pseudotumor cerebri due to primary antiphospholipid syndrome. She has normal findings on MR venography. Antiphospholipid syndrome should be considered in the differential diagnosis of pseudotumor cerebri, even in the patients without evidence of venous thrombosis on MR angiography.
Adolescent ; Angiography ; Antiphospholipid Syndrome* ; Diagnosis, Differential ; Female ; Humans ; Phlebography ; Pseudotumor Cerebri* ; Venous Thrombosis