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Background: The leading causes of death among the elderly with cognitive impairment are unknown. This study aims to estimate the suicide and accidental death rates on the basis of a clinical case registry of patients diagnosed with cognitive impairment. Methods: The target sample consisted of 10,169 patients diagnosed with dementia or mild cognitive impairment (MCI), who were evaluated at the Clinical Research Center for Dementia of Korea (CREDOS) from January 2005 to December 2013. Information about whether the patients had died from suicide or in any kind of accident by December 31, 2016, was obtained from the database of the National Statistical Office (NSO). The standardized mortality ratio (SMR) and Cox-regression analysis were performed for evaluating the risk of suicide and accidental death as identified by the ICD-10. Results: The average of the Clinical Dementia Rating Scale (CDR) score (0.68 vs 0.93) was lower, and the age at the time of study registration (71.42 vs 75.68 years) was younger in the suicidal death group, as compared to the accidental death group. The overall SMR for accidental death in cognitively impaired patients (1.44, 95% CI 1.22–1.71) was significantly higher than the general population. Later onset (1.43, 95% CI 1.20–1.71) and older age (2.21, 95% CI 1.04–4.68) increased the risk of accidental death in cognitively impaired patients. According to the dementia subtypes, the SMR for accidental death was higher in both Alzheimer's disease (1.72, 95% CI 1.36–2.14) and vascular dementia (2.14, 95% CI 1.27–3.38). Additionally, the SMR for accidental death showed an increasing tendency as the CDR score increased (mild 1.80, 95% CI 1.32–2.42, moderate 1.86, 95% CI 1.07–3.03, severe 3.32, 95% CI 1.08–7.76). Unemployment increased the risks of both suicide (3.71, 95% CI 1.54–8.95) and accidental death (2.09, 95% CI 1.20–3.63). Conclusions: Among people with cognitive impairment, the risk of death by suicide did not increase, whereas that of accidental death increased significantly. Preventive strategies for premature mortality in those with cognitive impairment should be implemented from the early stages and should include careful evaluation of the individual risk factors for each type of death. [ABSTRACT FROM AUTHOR]

Backgroud: Use of multifunctional drugs with neurotrophic supporting and oxidative stress suppressing activity may be considered a therapeutic strategy to protect or repair cellular damage caused during the progression of Alzheimer’s disease (AD). In this study, we investigated the therapeutic effects of aqueous extract of A. cochinchinesis root (AEAC), particularly its role as a nerve growth factor (NGF) stimulator and anti-oxidant in Tg2576 mice showing AD phenotypes of human. Methods: Tg2576 mice were received 100 mg/kg/day AEAC via oral administration, while mice in the Vehicle treated group received dH2O for 4 weeks. Non-Tg littermates were used as a control group. Following AEAC treatment for 4 weeks, NGF function, anti-oxidantive status, Aβ-42 peptide level, γ-secretase expression and neuronal cell functions were analyzed in the brain of Tg2576 mice. Results: AEAC containing flavonoids, phenols, saponins and protodioscin induced enhancement of NGF secretion and decreased intracellular ROS in the neuronal and microglial cell line. These effects as well as enhanced SOD levels were also detected in AEAC treated Tg2576 mice. The expression of p-Akt among downstream effectors of the high affinity NGF receptor was dramatically recovered in AEAC treated Tg2576 mice, while the expression of p75NTR was slightly recovered in the same group. Significant recovery on the level of Aβ-42 peptides and the expression of γ-secretase members including PS-2, APH-1 and NCT were detected in AEAC treated Tg2576 mice. Furthermore, AEAC treated Tg2576 mice showed decreased numbers of dead cells and suppressed acetyl choline esterase (AChE) activity. Conclusions: These results suggest that AEAC contribute to improving the deposition of Aβ-42 peptides and neuronal cell injuries during the pathological progression stage of AD in the brain of Tg2576 mice through increased NGF secretion and suppressed oxidative stress. [ABSTRACT FROM AUTHOR]