No abstract available.
Alzheimer Disease* ; Developing Countries* ; Primary Prevention*

The Ministry of Science and ICT and the Ministry of Health and Welfare of the Republic of Korea have organized the first National Committee for Dementia Research, to which all domestic experts in the field have been invited as they endeavor to achieve ‘national dementia liability’, which is one of the core national agenda items of the current Korean government. To make this initiative sustainable and bring dementia under control, we should not focus only on providing care and economic support to the family of patients with dementia. Instead, a large-scale, long-term research and development (R&D) strategy for dementia prevention, diagnosis, and therapy is warranted. This R&D project comprises several parts: 1) elucidation of the etiology and prevention of dementia, 2) innovative diagnostics for dementia, 3) tailored therapies for dementia, and 4) tangible and effective care for dementia. Given the fact that dementia is a very heterogeneous condition involving multiple pathogenic factors and typically having a chronic disease course, comprehensive and integrated approaches across various disciplines should be explored for primary, secondary, and tertiary prevention of this disease. With the success of this R&D project, the national dementia liability system will gain momentum and come into its own. Integrated efforts in terms of both policyrelated and scientific initiatives would allow us to take a step closer to realizing our shared goal of living in a world of dementia carefree.
Alzheimer Disease ; Chronic Disease ; Dementia ; Diagnosis ; Humans ; Republic of Korea ; Tertiary Prevention

Aging ; Alzheimer Disease ; diagnosis ; epidemiology ; prevention & control ; Humans ; Incidence ; Leisure Activities ; Psychological Tests

Vascular dementia is one of the few remediable causes of dementia among the eldery. Prevention of the disease can be best achieved by primary or secondary prevention of controllable risk factors for strokes. Therefore, early and accurate diagnosis of vascular cognitive impairment prior to the dementia stage is essential to the prevention and treatment of vascular dementia. Pharmacological and non-pharmacological methods for prevention of vascular dementia are listed in this article. Recent epidemiologic data, suggesting a direct correlation between vascular risk factors and Alzheimer type dementia, emphasized the importance of controlling vascular risk factors in the prevention of dementia. Treatment strategies for patients diagnosed as vascular dementia are also discussed. Several clinical trials for symptomatic improvement of vascular dementia are ongoing and their success can be a hope to patients with vascular dementia.
Alzheimer Disease ; Cognition Disorders ; Dementia ; Dementia, Vascular* ; Diagnosis ; Hope ; Humans ; Risk Factors ; Secondary Prevention ; Stroke

Alzheimer's disease(AD)is a central nervous system disease characterized by progressive cognitive dysfunction and memory loss.Increasing evidences suggest that β amyloid(Aβ)plays a critical role and may be a upstream molecule in AD pathogenesis involving both genetic and environmental factors.Aβ accumulation and its related inflammation are considered early events preceding neurodegeneration and neuronal loss in AD brain.However,all strategies and compounds targeting Aβ deposition have failed in clinical trials,implying complexity of AD pathogenesis.This article reviews Aβ hypothesis and its related mechanisms,pathophysiological process,and therapeutics of AD.
Alzheimer Disease ; pathology ; prevention & control ; therapy ; Amyloid beta-Peptides ; Brain ; physiopathology ; Humans

Alzheimer's disease (AD) is a multifactorial and heterogenic disorder. MiRNA is a class of non-coding RNAs with 19-22 nucleotides in length that can regulate the expression of target genes in the post-transcriptional level. It has been found that the miRNAome in AD patients is significantly altered in brain tissues, cerebrospinal fluid and blood circulation, as compared to healthy subjects. Experimental studies have suggested that expression changes in miRNA could drive AD onset and development via different mechanisms. Therefore, targeting miRNA expression to regulate the key genes involved in AD progression is anticipated to be a promising approach for AD prevention and treatment. Rodent AD models have demonstrated that targeting miRNAs could block biogenesis and toxicity of amyloid β, inhibit the production and hyper-phosphorylation of τ protein, prevent neuronal apoptosis and promote neurogenesis, maintain neural synaptic and calcium homeostasis, as well as mitigate neuroinflammation mediated by microglia. In addition, animal and human studies support the view that miRNAs are critical players contributing to the beneficial effects of cell therapy and lifestyle intervention to AD. This article reviews the most recent advances in the roles, mechanisms and applications of targeting miRNA in AD prevention and treatment based on rodent AD models and human intervention studies. The potential opportunities and challenges in clinical application of targeting miRNA for AD patients are also discussed.
Animals ; Humans ; MicroRNAs/genetics* ; Alzheimer Disease/prevention & control* ; Amyloid beta-Peptides ; Apoptosis ; Microglia

Alzheimer's disease (AD) is the leading cause of dementia, and the most prevalent neurodegenerative disease in the elderly. The prevalence of AD is predicted to rise as life expectancy grows across populations. The exact cause of this devastating disease is still unknown; however, it is an aging-related multi-factorial disorder, and growing evidence supports the contribution of modifiable environmental factors to unmodifiable factors such as gene and ageing itself. The recent advancement of methodologies and techniques for early diagnosis of AD facilitates the investigation of strategies to reduce the risk for AD progression in the earliest stages of the disease. Pharmacological attempts at curing, halting or modifying it have, by and large, been unsuccessful, and no breakthrough is seen in the near future. However, a lot of elements that seem to contribute to the disease such as risk factors have been identified, mainly from epidemiological and basic research studies. Many of these are amenable to lifestyle modification. Therefore, prevention in the preclinical stage is likely the most effective way to decrease the incidence of this age-associated dreadful neurodegenerative condition, and its associated burden for individuals and society. We provide an overview of modifiable risk factors for AD along with the supporting evidence.
Alzheimer Disease/epidemiology/*prevention & control ; Cognitive Therapy ; Dietary Supplements ; Health Behavior ; Humans ; Mind-Body Therapies ; Motor Activity ; Risk Factors

This article reviewed the beneficial effects of moderate voluntary physical exercise on brain health according to the studies on humans and animals, which includes improving psychological status and cognitive function, enhancing psychological well-being, decreasing the risks of Alzheimer's disease (AD) and dementia, and promoting the effects of antidepressant and anxiolytic. The possible underlying neurobiological mechanisms are involved up-active and down-active pathways. The up-active pathway is associated with enhancements of several neurotransmitters systems afferent to hippocampus, including norepinephrine (NE), serotonin (5-Hydroxytryptamine, 5-HT), acetylcholine (ACh) and gamma-aminobutyric acid (GABA). The down-active pathway is mainly concerned with up-regulation of the brain-derived neurotrophic factor (BDNF) and neurogenesis. It is suggested that NE activation via beta-adrenergic receptors may be essential for exercise-induced BDNF up-regulation. The possible intracellular signaling pathways of NE-mediated BDNF up-expression may be involved in GPCR-MAPK-PI-3K crosstalk and positive feedback.
Alzheimer Disease ; prevention & control ; Animals ; Brain ; physiology ; Dementia ; prevention & control ; Exercise ; physiology ; Humans ; Neurotransmitter Agents ; metabolism ; Physical Conditioning, Animal ; physiology ; Signal Transduction ; physiology

Alzheimer Disease ; drug therapy ; genetics ; prevention & control ; Amyloid beta-Peptides ; genetics ; Animals ; Disease Models, Animal ; Mice ; Mice, Transgenic ; Phytotherapy ; Presenilin-1 ; genetics

OBJECTIVEThe present study investigated the inhibitory effects of Chinese herb component sinapine on activity of acetylcholinesterase (AChE) in cerebral homogenate and blood serum of rats.

METHODAChE was prepared from cerebral homogenate and blood serum of rats, respectively. Acetylcholinesterase activity assay kit and Chromatometry were used to detect the AChE activity.

RESULTSinapine significantly inhibited AChE activity in vitro, with more effective on cerebral homogenate (IC50 3.66 micromol x L(-1)) than blood serum (IC50 22.1 micromol x L(-1)).

CONCLUSIONSinapine could significantly inhibit the cerebral AChE activity and may be a promising drug used for prevention and cure of Alzheimer's disease as a cholinesterase inhibitor.

Acetylcholinesterase ; blood ; metabolism ; Alzheimer Disease ; drug therapy ; prevention & control ; Animals ; Brain ; cytology ; enzymology ; Choline ; analogs & derivatives ; pharmacology ; therapeutic use ; Cholinesterase Inhibitors ; pharmacology ; therapeutic use ; Rats