Cognitive Frailty and Its Association with Nutrition and Depression in Community-Dwelling Older People.

BACKGROUND: Cognitive frailty is a condition where physical frailty and mild cognitive impairment (MCI) co-exist. It is associated with increased risk of dementia and dependency. Previous studies reported that malnutrition and depression are associated with physical frailty and MCI; however, their relationships with cognitive frailty remained to be explored. The aims of this study were to examine the association of nutrition and depression with cognitive frailty, in comparison to having physical frailty or MCI alone. METHODS: This study employed a cross-sectional design. Data collection was conducted in the community settings on the older people without dementia. Dependent variables were cognitive frailty, physical frailty, and MCI. The independent variables were depression and nutrition. Multi-nominal regression was employed to examine the relationships between the dependent and independent variables. The associations were adjusted by four known co-variates, including age, gender, education and APOE ε4 carrier status. RESULTS: A total of 185 participants were recruited from four community centres and one elderly hostel and completed the data collection. Approximately 44.9% of the older people with physical frailty and 82.5% of elderly with MCI belonged to cognitive frailty. Multi-nominal regression models showed that depression is positively associated with cognitive frailty and with physical frailty, but not associated with solely MCI. Nutrition is negatively associated with cognitive frailty, but not associated with physical frailty or MCI alone. CONCLUSION: Cognitive frailty is associated with malnutrition and depression. Therapeutic interventions managing depression and malnutrition may focus the older people with cognitive frailty to improve efficacy and cost-effectiveness.

Alzheimer's disease: insights for risk evaluation and prevention in the Chinese population and the need for a comprehensive programme in Hong Kong/China.

With the ageing of the global population, China is projected to be impacted significantly by the rising number of patients with Alzheimer's disease (AD). A cure for AD is not yet available, so society should be prepared for an increasing AD-related burden. In this review, we examine this impending problem and provide overviews on (a) the magnitude of the problem of AD in Hong Kong/China in the near future; (b) the genetic and lifestyle risk factors that contribute to AD; (c) current diagnostic approaches and the potential of newly discovered genetic biomarkers for early detection; (d) medications, non-pharmacological interventions, and possible preventive measures; and (e) the need for social and psychological care from the community. In Hong Kong, primary care and AD-related support for at-risk individuals, patients, and caregivers are inadequate. A joint effort from the medical community, government, universities, non-governmental organisations/charities, and industry should initiate the development of a long-term programme for AD. Finally, we outline recommendations for the relevant parties to consider.

Detection of animal viruses using nucleic acid sequence-based amplification (NASBA).

As seen in recent avian influenza outbreaks in Asia, prevention is the key to fighting infectious disease successfully. Efficient disease surveillance systems on the basis of molecular diagnostics will help monitor the emergence of viruses in the early stage and thus prompt containment measures can be in place to minimize disease spread. Here we describe and review molecular diagnostics focusing on nucleic acid sequence-based amplification (NASBA) technology in detecting viruses causing animal diseases, such as avian influenza, foot-and-mouth disease, and Newcastle disease. NASBA offers high sensitivity, specificity, accuracy, and speed of availability of results, and NASBA would be the most applicable molecular diagnostics for disease surveillance and control.

A NASBA method to detect high- and low-pathogenicity H5 avian influenza viruses.

Nucleic acid sequence-based amplification (NASBA) allows the rapid amplification of specific regions of nucleic acid obtained from a diverse range of sources. It is especially suitable for amplifying RNA sequences. A NASBA technique was developed that allows the detection of avian influenza A subtype H5 from allantoic fluid harvested from inoculated chick embryos. The amplified viral RNA is detected by electrochemiluminescence. The described NASBA technique is a specific, rapid, and sensitive method of detection of influenza A subtype H5 viruses. More importantly, it can be used to distinguish high- and low-pathogenicity strains of the H5 subtype.

Ischemia-induced apoptosis in primary cultures of astrocytes.

Astrocytes participate in a wide variety of important physiological processes and pathological insults, including ischemia. Information on the mechanism of astroglial injury and death during ischemic insult, however, is scarce. In this study, we investigated the mode of astrocytic cell death using an in vitro ischemic model. Cultured astrocytes exhibited several distinct morphological and biochemical features of apoptosis under ischemia. At 4 h of ischemia, Annexin V staining demonstrated an early commitment of some astrocytes to apoptosis. Condensed nuclei became visible from 4 h and the number increased with ischemic incubation time. Electron microscopy showed compacted and segregated chromatin along the edges of nuclear membranes. The number of TUNEL-positive nuclei and the degree of DNA laddering increased with ischemic incubation. Caspase-3, but not caspase-1, activity was increased in ischemia-injured astrocytes. Swollen mitochondria and vacuoles found in some cells with chromatin condensation indicated that these apoptotic-like cells might die of necrosis. The results imply that astrocytes are capable of undergoing apoptosis without the presence of other cell types, such as neurons. Ischemia can induce apoptosis in astrocytes contributing to the pathogenesis of ischemic injury in the CNS.

Astrocytes produce and release interleukin-1, interleukin-6, tumor necrosis factor alpha and interferon-gamma following traumatic and metabolic injury.

The brain is no longer considered immune-privileged due to its capability of producing cytokines in response to neurotrauma; however, the cellular sources of cytokines have not been defined. This study focused on the production of four inflammatory cytokines, interleukin-1 (IL-1alpha), interleukin-6 (IL-6), tumor necrosis factor alpha (TNFalpha), and interferon gamma (IFN-gamma) in primary culture of astrocytes under two different injury models which simulated in vivo mechanical trauma (scratch injury) and ischemia. Results demonstrated that astrocytes after scratch injury were positively immunostained with IL-1alpha, IL-6, and TNFalpha. A slot-blot study of culture media showed that the release of IL-1alpha, IL-6, TNFalpha, and IFN-gamma by astrocytes subsequent to scratch and ischemic injury reached approximately twice the control values. The temporal expression of these cytokines was different for the two models. All four cytokines began to increase 1 h postscratch and remained at high levels throughout the experiment. In the ischemic model, however, the increase of cytokine expression was delayed until 4-8 h of ischemia, when sharp increases were seen in all four cytokines. In this culture system, the exogenous influence of blood-borne factors and leukocytes, which occur with in vivo trauma and ischemia, was eliminated. Accordingly, the cytokines detected in the culture media were derived from astrocytes. This study provides the first evidence that astrocytes, without the influence from other cell types, can produce and release cytokines following mechanical and ischemic injury.

Expression of interleukin-1 alpha, tumor necrosis factor alpha and interleukin-6 genes in astrocytes under ischemic injury.

Astrocytes form an integral part of the blood brain barrier and are the first cell type in the central nervous system to encounter insult if there is an ischemic attack. The immunologic reaction of astrocytes to an ischemic insult would be affective to the subsequent responses of other nerve cells. We previously showed that ischemia caused an increase in the levels of interleukin 1alpha (IL-1alpha), tumor necrosis factor alpha (TNF alpha), and interleukin 6 (IL-6) in the culture medium of mouse cerebral cortical astrocyte. We did not have evidence on the source of these cytokines. This study aimed to investigate the expressions of these cytokine mRNAs in the astrocytes under ischemia. Results demonstrated that ischemia could induce necrosis and apoptosis in astrocytes. By using the RT-PCR method, we demonstrated for the first time that the mRNA levels of IL-1alpha, TNF alpha and IL-6 in normal astrocyte was very low, but their expressions could be induced quickly under ischemia. These cytokines might be interactive as indicated by the difference in time course of their expressions, with IL-1alpha being the earliest and IL-6 being the latest. The result provided some understanding of the induction and progression of these immunologic responses in astrocytes under ischemia. It also supported our previous findings that astrocytes contributed to the cytokines released under ischemia.