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Abstract Background Inflammation and altered lipid dyshomeostasis have been implicated in the pathogenesis of Alzheimer's disease and vascular dementia. Objective To determine if there are any associations between dietary patterns, plasma lipid profiles, and inflammatory potential in a vascular dementia cohort. Methods One hundred fifty participants (36 subjects with Vascular Dementia and 114 healthy controls) from two Australian teaching hospitals completed a cross‐sectional survey examining their dietary and lifestyle patterns. Each participant's diet was further evaluated using the Empirical Dietary Inflammatory Index. Some participants also donated blood samples for lipidomic analysis. Results After adjusting for age, education, and socioeconomic status, participants with vascular dementia tend to have higher lipid profiles, do less exercise, and engage less frequently in social interaction, educational, or reading activities. They also tend to consume more deep‐fried food and full‐fat dairy compared to control subjects. However, there was no difference in Empirical Dietary Inflammatory Index between the two groups after adjusting for age, education, and socioeconomic status. Conclusion Our findings suggest a graded inverse association between healthy lifestyle factors and vascular dementia.

Abstract Objective WeiNaoKang (or SaiLuoTong) is an herbal formula consisting of ginkgo, ginseng, and saffron. Our objective was to investigate if WeiNaoKang could improve cognitive function and cerebral perfusion in patients suffering from vascular dementia. Methods A 16‐week randomized double‐blind, placebo‐controlled trial was carried out in the setting of a memory disorder clinic at a single center. Patients with vascular dementia diagnosed clinically but supported by imaging and other investigations were invited to participate. The diagnoses were based on the National Institute of Neurological Disorders and Stroke/Association Internationale pour la Recherche et l'Enseignement en Neurosciences (NINDS‐AIREN) criteria. An independent blinded assessor evaluated the effects of the formula. Intervention group was compared to the control group. A subgroup of participants was randomly chosen for further evaluation of cerebral perfusion by single photon emission computed tomography scans post‐treatment. Results Both groups were comparable in age (mean = 74 ± 7.2 years in the placebo group and 75 ± 7.4 in the intervention group) and in other demographics. Sixty‐two participants were included in final analysis. Alzheimer's Disease Assessment Scale – Cognitive Portion (ADAS‐cog) was the primary outcome. By week 16, the mean ADAS‐cog reduced from 24.48 to 20.30 (mean reduction = 4.18) for those in the treatment group, and from 18.98 to 17.81 (mean reduction = 1.18) for those in the placebo group. The difference in mean reduction of ADAS‐cog was −3.00 (95% confidence interval [CI] = −4.910 to −1.100) in favor of the treatment group. Secondary outcomes of activities of daily living and quality of life measures also showed significant difference. In the perfusion scan analysis, the difference in the change in cerebral blood flow (t‐scores) pre‐ and post‐treatment between the intervention group (n = 7) and the placebo group (n = 11) was statistically significant (P

Abstract Objective The aim of this study was to evaluate the effectiveness and identify factors predictive of home discharge in a cohort of patients admitted to the residential Transitional Aged Care Program (r‐TACP) after a stay in an acute hospital. Methods A retrospective observational cohort study of patients admitted to a single r‐TACP unit between 1 January 2014 and 31 December 2017 was carried out. Baseline patient characteristics and discharge outcomes were analyzed. Results Three hundred sixty‐nine patients were admitted during the study period. The discharge outcomes were as follows: 68% returned home, 17% went onto residential care, 14% were readmitted to hospital, and 1% died. Factors associated with not returning home were increased age, increased comorbidities, and lower Barthel Index on admission to the r‐TACP. Conclusion Our r‐TACP is an effective program that successfully returns the majority (67.8%) of older patients home after an acute hospital admission. Older patients with greater comorbidities and poorer baseline functional status in our program were less likely to return home.

Abstract In this mini-review, we summarize recent findings relating to the prion-like propagation of α-synuclein (α-syn) and the development of novel therapeutic strategies to target synucleinopathy in Parkinson’s disease (PD). We link the Braak’s staging hypothesis of PD with the recent evidence from in-vivo and in-vitro studies for the prion-like cell-to-cell propagation of α-syn (via exocytosis and endocytosis). The classical accumulation of aggregated α-syn in PD may result from an increased production or a failure in the mechanisms of clearance of α-syn. We discuss novel agents, currently in clinical trial for PD including the ones that impact the aggregation of α-syn and others that interfere with α-syn endocytosis as a means to target the progression of the disease.

Discovering genes following Medelian inheritance, such as autosomal dominant-synuclein and leucine-rich repeat kinase 2 gene, or autosomal recessive Parkin, P-TEN-induced putative kinase 1 gene and Daisuke-Junko 1 gene, has provided great insights into the pathogenesis of Parkinson’s disease (PD). Genes found to be associated with PD through investigating genetic polymorphisms or via the whole genome association studies suggest that such genes could also contribute to an increased risk of PD in the general population. Some environmental factors have been found to be associated with genetic factors in at-risk patients, further implicating the role of gene-environment interactions in sporadic PD. There may be confusion for clinicians facing rapid progresses of genetic understanding in PD. After a brief review of PD genetics, we will discuss the insight of new genetic discoveries to clinicians, the implications of ethnic differences in PD genetics and the role of genetic testing for general clinicians managing PD patients.

Vast changes have occurred in China in the last five years since the decision of the Chinese Government to reform its health system. Many district and community hospitals in the city have been converted into community health centers. The hospital-based doctors who used to work in these centers are being retrained to become general practitioners (GPs). The reform had encountered many problems. The community has not embraced the concept of general practice readily. Lack of fair remuneration and lack of recognition of the importance of the reform by bureaucrats of local government are other problems encountered. The Ministry of Health meanwhile has also introduced a system of retraining hospital-based doctors to become GPs. A medical education curriculum for GPs has been developed. A nationwide network of GP training centers is progressively being formed. The GP training program has also extended to under-graduate medical students. Despite the progress made, many difficulties remained especially in regional areas. The speed and quality of GP training in wealthy, developed places is better than poorer regional areas. The issuing of national license and registration examinations for GPs has not been synchronized with GP training, leading to uneven standard of GP practice. Staff morale is also poor due to the lack of chance for promotion and professional development. Although a number of strategies have been proposed to improve the situation, problems are enormous that China may welcome international collaboration.

The purpose of this paper is to elaborate criteria by which the principles of curriculum reform can be judged. To this end, the paper presents an overview of standard critiques of medical education and examines the ways medical curriculum reforms have responded to these critiques. The paper then sets out our assessment of these curriculum reforms along three parameters: pedagogy, educational context, and knowledge status. Following on from this evaluation of recent curriculum reforms, the paper puts forward four criteria with which to gauge the adequacy medical curriculum reform. These criteria enable us to question the extent to which new curricula incorporate methods and approaches for ensuring that its substance: overcomes the traditional opposition between clinical and resource dimensions of care; emphasizes that the clinical work needs to be systematized in so far as that it feasible; promotes multi-disciplinary team work, and balances clinical autonomy with accountability to non-clinical stakeholders.

Background: Because apolipoprotein E (apoE) and lipopoprotein lipase (LPL) polymorphisms interact with each other and with other factors to affect lipid metabolism, we sought to determine their separate and combined effects in association with ischemic vascular disease. Methods: We performed a case-control study of 816 subjects: 246 acute ischemic stroke patients, 234 acute myocardial infarction patients, and 336 controls. APOE exon 4 and LPL S447X genotypes were determined. Results: APOE ɛ2 and ɛ4 homozygotes were increased in stroke (4.5% vs. 1.0%, p=0.008), while in myocardial infarction the ɛ4 allele was increased (12.6% vs. 9.5%, p=0.006) but ɛ2 was decreased (3.7% vs. 12.1%, p=0.000006). For subjects with either APOE ɛ2 or ɛ4 alleles, LPL X alleles were increased in vascular disease (OR=2.2, p=0.01). LPL X alleles displayed opposite tendencies toward association with disease when subjects were divided by sex, smoking, or APOE genotype. Meta-analysis and regression analysis of previous studies supported the sex and smoking dichotomies. Conclusion: This is the first report of an association of vascular disease with an interaction of APOE exon 4 and LPL S447X genotypes. Therefore, APOE genotypes and LPL S447X interactions with apoE, sex, and smoking may affect the risk of myocardial infarction and ischemic stroke. [ABSTRACT FROM AUTHOR]