• Journal of Medicine and Life Science
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• v.15 no.2
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• pp.89-94
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• 2018

Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is inherited microangiopathy caused by mutations in the Notch3 gene. Typical findings from brain magnetic resonance imaging (MRI) include subcortical lacunes, extensive white matter change and cerebral microbleeds(CMBs). CMBs are indicative of bleeding-prone microangiopathy. Despite some studies investigating the association between lacunes and cognitive dysfunction in CADASIL, few studies have examined the relationship between cognitive dysfunction and CMBs. We sought to assess whether CMBs are associated with cognitive dysfunction in CADASIL. This study enrolled 83 consecutive patients with CADASIL between April 2012 and January 2014. Their degree of cognitive dysfunction was assessed by the Korean version of the CERAD neuropsychological assessment battery, digit span test, and the Stroop test. A 3.0-T MRI was used to obtain T1-weighted, fluid-attenuated inversion recovery, and susceptibility weighted images. In multiple logistic regression analysis, the grade of CMBs influenced tests of memory dysfunction (p=0.003). Three or more lacunes correlated with dysfunction in the executive domain (p=0.013) and attention domain (p=0.005). White matter hyperintensity (WMH) was an independent predictor of executive dysfunction (p=0.001). These findings suggest that in addition to lacunes, CMBs and WMHs may be useful imaging markers to associated with cognitive dysfunction in CADASIL.

• Sleep Medicine and Psychophysiology
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• v.4 no.2
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• pp.140-146
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• 1997

Sleep-related breathing disorders, especially sleep apnea syndrome are complicated by neuropsychiatric dysfunction such as excessive daytime sleepiness, cognitive dysfunction, and depression. As the determinants of daytime sleepiness, sleep fragmentation is more influential than nocturnal hypoxia. Daytime sleepiness can be improved by continuous positive airway pressure (CPAP) or surgery in up to 95% of the treated subjects. Both sleepiness and nocturnal hypoxia would cause cognitive dysfunction. While impairments in attention and verbal memory are more related with sleepiness and prominent in mild to moderate sleep apnea syndrome (SAS), impairments in general intellectual function and executive function are more related with nocturnal hypoxia and prominent in severe SAS. Several cognitive deficits related with nocturnal hypoxia may be irreversible despite CPAP or surgical treatments. So, early detection and early appropriate treatment of SAS would prevent sleepiness and cognitive deterioration.

• Journal of Digital Convergence
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• v.15 no.3
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• pp.393-403
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• 2017

The purpose of this study was to investigate the degree of cognitive impairment for the elders taking part in activities at senior community center and to identify the multiple factors affecting the cognitive dysfunction of them. Data were collected for the 375 elders taking part in activities at senior community center at 4 different areas of dong, up, and myun of C-city from June 2016 to July 2016, and their general characteristics as well as health-related characteristics, depression, and cognitive dysfunction were investigated and analyzed. The results of this study showed that cognitive dysfunction was affected by the age, education, economic support, history of stroke, and exercise. The risk of cognitive dysfunction was 3.50 times higher in patients over 80 years old than patients below 74 years old(p=.002), and the lower the level of education showed the higher the risk of cognitive dysfunction(p=.036)(p<.001). In addition, the risk of cognitive dysfunction was low in the absence of a history of stroke(p=.033), and the risk of cognitive dysfunction increased by 1.84 times if they do not exercise(p=.044). Based on the present study, It is required to consider the risk factors for cognitive dysfunction efforts to prevent and manage cognitive impairment before the onset of cognitive dysfunction.

• Journal of Yeungnam Medical Science
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• v.40 no.3
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• pp.225-232
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• 2023

Cognitive dysfunction is relatively less considered a complication of hypertension. However, there is sufficient evidence to show that high blood pressure in middle age increases the risk of cognitive decline and dementia in old age. The greatest impact on cognitive function in those with hypertension is on executive or frontal lobe function, similar to the area most damaged in vascular dementia. Possible cognitive disorders associated with hypertension are vascular dementia, Alzheimer disease, and Lewy body dementia, listed in decreasing strength of association. The pathophysiology of cognitive dysfunction in individuals with hypertension includes brain atrophy, microinfarcts, microbleeds, neuronal loss, white matter lesions, network disruption, neurovascular unit damage, reduced cerebral blood flow, blood-brain barrier damage, enlarged perivascular damage, and proteinopathy. Antihypertensive drugs may reduce the risk of cognitive decline and dementia. Given the high prevalence of dementia and its impact on quality of life, treatment of hypertension to reduce cognitive decline may be a clinically relevant intervention.

• Journal of The Korean Society of Clinical Toxicology
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• v.14 no.2
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• pp.115-121
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• 2016

Purpose: Because carbon monoxide (CO)-intoxicated patients with an alert mental status and only mild cognitive dysfunction may be inadequately assessed by traditional bedside neurologic examination in the emergency department (ED), they may not receive appropriate treatment. Methods: We retrospectively investigated the incidence and features of cognitive dysfunction using the Korean version of the Mini-Mental State Examination (MMSE-K) in ED patients with CO poisoning with alert mental status. We conducted a retrospective review of 43 consecutive mild CO poisoned patients with a Glasgow Coma Scale score of 15 based on documentation by the treating emergency physician in the ED between July 2014 and August 2015. Results: Cognitive dysfunction, defined as a score of less than 24 in the MMSE-K, was diagnosed in six patients (14%) in the ED. In the MMSE-K, orientation to time, memory recall, and concentration/calculation showed greater impairments. The mean age was significantly older in the cognitive dysfunction group than the non-cognitive dysfunction group (45.3 yrs vs. 66.5 yrs, p<0.001). Among the initial symptoms, experience of a transient change in mental status before ED arrival was significantly more common in the cognitive dysfunction group (32.4% vs. 100%, p=0.003). Conclusion: Patients with CO poisoning and an alert mental status may experience cognitive dysfunction as assessed using the MMSE-K during the early stages of evaluation in the ED. In the MMSE-K, orientation to time, memory recall, and concentration/calculation showed the greatest impairment.

• Journal of Yeungnam Medical Science
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• v.36 no.3
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• pp.183-191
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• 2019

Some patients with type 1 and type 2 diabetes mellitus (DM) present with cognitive dysfunctions. The pathophysiology underlying this complication is not well understood. Type 1 DM has been associated with a decrease in the speed of information processing, psychomotor efficiency, attention, mental flexibility, and visual perception. Longitudinal epidemiological studies of type 1 DM have indicated that chronic hyperglycemia and microvascular disease, rather than repeated severe hypoglycemia, are associated with the pathogenesis of DM-related cognitive dysfunction. However, severe hypoglycemic episodes may contribute to cognitive dysfunction in high-risk patients with DM. Type 2 DM has been associated with memory deficits, decreased psychomotor speed, and reduced frontal lobe/executive function. In type 2 DM, chronic hyperglycemia, long duration of DM, presence of vascular risk factors (e.g., hypertension and obesity), and microvascular and macrovascular complications are associated with the increased risk of developing cognitive dysfunction. The pathophysiology of cognitive dysfunction in individuals with DM include the following: (1) role of hyperglycemia, (2) role of vascular disease, (3) role of hypoglycemia, and (4) role of insulin resistance and amyloid. Recently, some investigators have proposed that type 3 DM is correlated to sporadic Alzheimer's disease. The molecular and biochemical consequences of insulin and insulin-like growth factor resistance in the brain compromise neuronal survival, energy production, gene expression, plasticity, and white matter integrity. If patients claim that their performance is worsening or if they ask about the effects of DM on functioning, screening and assessment are recommended.

• Annals of Geriatric Medicine and Research
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• v.22 no.4
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• pp.176-183
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• 2018

Background: Although the frequency and intensity of headaches decrease in older adults, headaches in this population are still an important neurological disorder. The purpose of this study was to investigate the associations of headache characteristics in older adults with the development of cardiovascular disease and cognitive dysfunction. Methods: We prospectively enrolled 125 older (${\geq}65$ years old) patients with headache who were making their first visit to outpatient clinics and who had no prior history of cognitive dysfunction from 11 hospitals in Korea between August 2014 and February 2015. We investigated the occurrence of newly developed/or recurrent headache, cardiovascular disease, cognitive dysfunction, and poor functional outcomes. Results: The mean age of all included patients was 72.6 years, 68.8% were women, and 43 (34.4%) had newly developed/or recurrent headache during follow-up. During a median follow-up of 31 months (interquartile range, 28-34 months), 21 participants (16.8%) experienced cardiovascular disease, and 26 (20.8%) developed cognitive dysfunction. Upon multivariate analysis and after adjusting for sex, age, and other factors, presence of newly developed/or recurrent headache was found to be associated with cardiovascular disease (hazard ratio [HR], 4.03; 95% confidence interval [CI], 1.28-12.61; p=0.017) and frequency of headache for the recent 3 months was related with cognitive dysfunction (HR, 1.05; 95% CI, 1.00-1.09; p=0.017) and poor functional outcomes (HR, 1.06; 95% CI, 1.01-1.11; p=0.011). Conclusion: Our study demonstrated that there is an increased risk of cardiovascular disease, cognitive dysfunction, and poor functional outcomes in older patients with frequent, newly developed, or recurrent headache.

• BMB Reports
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• v.54 no.6
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• pp.295-304
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• 2021

Olfactory neuropathology is a cause of olfactory loss in Alzheimer's disease (AD). Olfactory dysfunction is also associated with memory and cognitive dysfunction and is an incidental finding of AD dementia. Here we review neuropathological research on the olfactory system in AD, considering both structural and functional evidence. Experimental and clinical findings identify olfactory dysfunction as an early indicator of AD. In keeping with this, amyloid-β production and neuroinflammation are related to underlying causes of impaired olfaction. Notably, physiological features of the spatial map in the olfactory system suggest the evidence of ongoing neurodegeneration. Our aim in this review is to examine olfactory pathology findings essential to identifying mechanisms of olfactory dysfunction in the development of AD in hopes of supporting investigations leading towards revealing potential diagnostic methods and causes of early pathogenesis in the olfactory system.

• Biomolecules & Therapeutics
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• v.22 no.3
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• pp.176-183
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• 2014

Cognitive impairment is a result of dementia of diverse causes, such as cholinergic dysfunction and Alzheimer's disease (AD). Houttuynia cordata Thunb. (Saururaceae) has long been used as a traditional herbal medicine. It has biological activities including protective effects against amyloid beta ($A{\beta}$) toxicity, via regulation of calcium homeostasis, in rat hippocampal cells. To extend previous reports, we investigated the effects of water extracts of H. cordata herb (HCW) on tauopathies, also involving calcium influx. We then confirmed the effects of HCW in improving memory impairment and neuronal damage in mice with Ab-induced neurotoxicity. We also investigated the effects of HCW against scopolamine-induced cholinergic dysfunction in mice. In primary neuronal cells, HCW inhibited the phosphorylation of tau by regulating p25/p35 expression in $A{\beta}$-induced neurotoxicity. In mice with $A{\beta}$-induced neurotoxicity, HCW improved cognitive impairment, as assessed with behavioral tasks, such as novel object recognition, Y-maze, and passive avoidance tasks. HCW also inhibited the degeneration of neurons in the CA3 region of the hippocampus in Ab-induced neurotoxicity. Moreover, HCW, which had an $IC_{50}$ value of $79.7{\mu}g/ml$ for acetylcholinesterase inhibition, ameliorated scopolamine-induced cognitive impairment significantly in Y-maze and passive avoidance tasks. These results indicate that HCW improved cognitive impairment, due to cholinergic dysfunction, with inhibitory effects against tauopathies and cholinergic antagonists, suggesting that HCW may be an interesting candidate to investigate for the treatment of AD.

• Journal of Veterinary Clinics
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• v.40 no.6
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• pp.408-413
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• 2023

The incidence of canine cognitive dysfunction syndrome (CCDS), a prominent geriatric disease, is increasing because of the extended lifespan of companion animals. Various complementary therapies have been proposed for the management of CCDS. This study evaluated the clinical efficacy of the Brain Six Complex Extract^ⓒ in dogs with cognitive dysfunction syndrome (CDS). Fifteen dogs with CDS were included, and four to five drops of Brain Six Complex Extract^ⓒ, composed of herbal extracts, were applied around the dorsal neck of all dogs twice daily for 1-3 months. Clinical efficacy was evaluated using the CCDS scale, and serum β-amyloid oligomer concentrations were measured before and after administration of the extract. The CCDS scale score significantly decreased after administration in dogs with CDS (p = 0.0313), compared to pre-administration levels. Although the serum β-amyloid oligomer concentration decreased after administration, the change was not statistically significant (p > 0.05). A notable decrease was observed between pre- and post-administration in dogs with β-amyloid levels >300 pg/mL (p = 0.0313). The laboratory results showed no remarkable adverse effects of the extract. This study suggests that Brain Six Complex Extract^ⓒ extract could be an adjunctive treatment for dogs with CDS.