oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
整合医学对老年痴呆发病机制的探讨
A discussion on pathogenesis of senile dementia based onholistic integrated medicine
 [PDF]

李琦,蒋宏岩
- , 2016,
Abstract: 整合医学显现人体存在以肺为中心的静脉血自然上行、动脉血自然下行运动。在血液这一上行下行的运动过程中,又可见人体摄取的能量运行路径,肝门静脉吸收的营养成分上行入心肺,转化为动脉血后分布至大脑及全身。人体进入老年后,心肺功能衰退,将导致肝门静脉血液淤滞堆积,影响富含营养的肝门静脉血上行分布至大脑,长此以往,可造成由于心肺动力功能衰退引起的大脑渐进性营养不良,导致老年痴呆的发生。老年痴呆是一种自然生理现象。
Based on holistic integrated medicine, it was found that lungs were the center of ascending and descendingblood motion system in human body. During the blood movement, we can see the running path of energy intaken by humanbody. The hepatic portal vein absorbs nutrients, and the nutrients go upward into heart and lung along with the blood. Afterthe blood transforms into arterial blood, it runs into the brain and other places in human body. The functions of heart andlung in old people are declining, which causes the blood stasis or clot in hepatic portal vein and hinders the venous bloodfrom carrying the nutrients into the brain. If things continue this way, it may induce cerebral progressive dystrophy, andeven senile dementia. Senile dementia is a kind of natural physiological event
Traditional Chinese Medicine for Senile Dementia
Zhihong Lin,Jie Gu,Jin Xiu,Tingyan Mi,Jie Dong,Jyoti Kumar Tiwari
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/692621
Abstract: Traditional Chinese Medicine (TCM) has a 3000 years' history of human use. A literature survey addressing traditional evidence from human studies was done, with key result that top 10 TCM herb ingredients including Poria cocos, Radix polygalae, Radix glycyrrhizae, Radix angelica sinensis, and Radix rehmanniae were prioritized for highest potential benefit to dementia intervention, related to the highest frequency of use in 236 formulae collected from 29 ancient Pharmacopoeias, ancient formula books, or historical archives on ancient renowned TCM doctors, over the past 10 centuries. Based on the history of use, there was strong clinical support that Radix polygalae is memory improving. Pharmacological investigation also indicated that all the five ingredients mentioned above can elicit memory-improving effects in vivo and in vitro via multiple mechanisms of action, covering estrogen-like, cholinergic, antioxidant, anti-inflammatory, antiapoptotic, neurogenetic, and anti-Aβ activities. Furthermore, 11 active principles were identified, including sinapic acid, tenuifolin, isoliquiritigenin, liquiritigenin, glabridin, ferulic acid, Z-ligustilide, N-methyl-beta-carboline-3-carboxamide, coniferyl ferulate and 11-angeloylsenkyunolide F, and catalpol. It can be concluded that TCM has a potential for complementary and alternative role in treating senile dementia. The scientific evidence is being continuously mined to back up the traditional medical wisdom.
Present Situation of Research on Treatment of Senile Dementia by Traditional Chinese Medicine
中医药治疗老年期痴呆的研究现状

Zhu Yuelan,Pei Qinghua,Tang Qisheng,
朱跃岚
,裴清华,唐启盛

世界科学技术-中医药现代化 , 2002,
Abstract: With the change of disease varieties and the increase of life expectancy of human beings, the morbidity rates of senile dementia are increasing year by year, which has become a sort of commonly - and frequently - encountered disease and difficult to cure. This paper reviews the nomenclature of the symptoms and signs, the etiology and pathogenesis and the therapeutic rule of senile dementia as well as the present situation of its study through traditional Chinese medicine.
Ion Channels and Zinc: Mechanisms of Neurotoxicity and Neurodegeneration  [PDF]
Deborah R. Morris,Cathy W. Levenson
Journal of Toxicology , 2012, DOI: 10.1155/2012/785647
Abstract: Ionotropic glutamate receptors, such as NMDA, AMPA and kainate receptors, are ligand-gated ion channels that mediate much of the excitatory neurotransmission in the brain. Not only do these receptors bind glutamate, but they are also regulated by and facilitate the postsynaptic uptake of the trace metal zinc. This paper discusses the role of the excitotoxic influx and accumulation of zinc, the mechanisms responsible for its cytotoxicity, and a number of disorders of the central nervous system that have been linked to these neuronal ion channels and zinc toxicity including ischemic brain injury, traumatic brain injury, and epilepsy. 1. Introduction Although zinc is clearly an essential trace element that is required for the function of hundreds of enzymes and DNA-binding transcription factors, excessive zinc has long been implicated in processes leading to cellular damage. In the central nervous system large amounts of zinc can enter postsynaptic neurons through a variety of ion channels including glutamate receptors and voltage-gated calcium channels. This paper will first discuss the cellular pools of zinc, the mechanisms that appear to be responsible for the accumulation of neuronal zinc, and then outline the current hypotheses about how excess zinc exploits ion channels and other mechanisms to produce neurotoxicity in the hippocampus, amygdala, and cortex under pathological conditions. With these mechanisms in mind we will then discuss relevant clinical situations such as traumatic brain injury, ischemic injury (stroke), and epilepsy, where excess zinc accumulation can lead to neurodegeneration. 2. Neurotoxic Zinc: Cellular Sources and Routes of Entry 2.1. Sources of Neurotoxic Zinc While a majority of zinc in the central nervous system (CNS) is tightly bound to zinc-dependent enzymes and other proteins, approximately 10% is “free” or “chelatable” zinc which is not associated with proteins or aminoacid ligands. Under pathological conditions, free zinc appears to participate in the neurotoxic accumulation of zinc in neurons. In normal neurons, free zinc is predominately localized to the presynaptic vesicles of glutamatergic neurons [1, 2]. Free zinc has also been colocalized to GABA and glycine containing murine neurons [3]. Regions rich in vesicular free zinc include the mossy fibers of the hippocampus, the amygdala, and the olfactory bulb. “Zincergic” neurons are also abundant in the cortex [4]. In addition to the large pool of vesicular zinc, there is clear evidence for additional intracellular pools of zinc that can be liberated to form free zinc.
Zinc Metalloproteinases and Amyloid Beta-Peptide Metabolism: The Positive Side of Proteolysis in Alzheimer's Disease  [PDF]
Mallory Gough,Catherine Parr-Sturgess,Edward Parkin
Biochemistry Research International , 2011, DOI: 10.1155/2011/721463
Abstract: Alzheimer's disease is a neurodegenerative condition characterized by an accumulation of toxic amyloid beta- (A -)peptides in the brain causing progressive neuronal death. A -peptides are produced by aspartyl proteinase-mediated cleavage of the larger amyloid precursor protein (APP). In contrast to this detrimental “amyloidogenic” form of proteolysis, a range of zinc metalloproteinases can process APP via an alternative “nonamyloidogenic” pathway in which the protein is cleaved within its A region thereby precluding the formation of intact A -peptides. In addition, other members of the zinc metalloproteinase family can degrade preformed A -peptides. As such, the zinc metalloproteinases, collectively, are key to downregulating A generation and enhancing its degradation. It is the role of zinc metalloproteinases in this “positive side of proteolysis in Alzheimer's disease” that is discussed in the current paper. 1. Introduction Alzheimer’s disease (AD) is the leading form of dementia in the elderly, accounting for some two-thirds of all cases and exhibiting a prevalence of 5% in individuals older than 65 years. The disease is clinically characterized by a progressive cognitive impairment, including impaired decision making, orientation and judgement often accompanied, in the later stages, by psychobehavioural disturbances and language impairment. AD was originally described in 1906 by the German psychiatrist and neuropathologist, Alois Alzheimer, but it was his coworker, Emil Kraepelin who first coined the term “Alzheimer’s disease” [1]. What Alzheimer described were what we now know as the two major pathological hallmarks in the brains of AD-afflicted individuals, amyloid (also known as senile) plaques and neurofibrillary tangles (NFTs) [2]. At the molecular level, NFTs are composed of tau, a microtubule-associated protein which, in AD, becomes hyperphosphorylated and forms insoluble intracellular fibrils [3]. Amyloid plaques, on the other hand, are extracellular structures composed of 38–43 amino acid peptides called amyloid beta (A )-peptides. Although it is important to appreciate that AD is a multifactorial disease [4], a key theory as to disease causation is that of the “amyloid cascade hypothesis” whereby A -peptides are the leading cause of toxicity to neurons [5]. The initial version of the hypothesis proposed that mature amyloid fibrils and plaques in the brain were responsible for the observed neurotoxicity, but more recent incarnations point towards the earlier stage, smaller soluble A aggregates being the primary cause of AD [6, 7]. Whatever
HIV Neurotoxicity: Potential Therapeutic Interventions
David R. Wallace
Journal of Biomedicine and Biotechnology , 2006, DOI: 10.1155/jbb/2006/65741
Abstract: Individuals suffering from human immunodeficiency virus type 1 (HIV-1) infection suffer from a wide range of neurological deficits. The most pronounced are the motor and cognitive deficits observed in many patients in the latter stages of HIV infection. Gross postmortem inspection shows cortical atrophy and widespread neuronal loss. One of the more debilitating of the HIV-related syndromes is AIDS-related dementia, or HAD. Complete understanding of HIV neurotoxicity has been elusive. Both direct and indirect toxic mechanisms have been implicated in the neurotoxicity of the HIV proteins, Tat and gp120. The glutamatergic system, nitric oxide, calcium, oxidative stress, apoptosis, and microglia have all been implicated in the pathogenesis of HIV-related neuronal degeneration. The aim of this review is to summarize the most recent work and provide an overview to the current theories of HIV-related neurotoxicity and potential avenues of therapeutic interventions to prevent the neuronal loss and motor/cognitive deficits previously described.
HIV Neurotoxicity: Potential Therapeutic Interventions  [cached]
David R. Wallace
Journal of Biomedicine and Biotechnology , 2006,
Abstract: Individuals suffering from human immunodeficiency virus type 1 (HIV-1) infection suffer from a wide range of neurological deficits. The most pronounced are the motor and cognitive deficits observed in many patients in the latter stages of HIV infection. Gross postmortem inspection shows cortical atrophy and widespread neuronal loss. One of the more debilitating of the HIV-related syndromes is AIDS-related dementia, or HAD. Complete understanding of HIV neurotoxicity has been elusive. Both direct and indirect toxic mechanisms have been implicated in the neurotoxicity of the HIV proteins, Tat and gp120. The glutamatergic system, nitric oxide, calcium, oxidative stress, apoptosis, and microglia have all been implicated in the pathogenesis of HIV-related neuronal degeneration. The aim of this review is to summarize the most recent work and provide an overview to the current theories of HIV-related neurotoxicity and potential avenues of therapeutic interventions to prevent the neuronal loss and motor/cognitive deficits previously described.
Iron and Mechanisms of Neurotoxicity
Gabriela A. Salvador,Romina M. Uranga,Norma M. Giusto
International Journal of Alzheimer's Disease , 2011, DOI: 10.4061/2011/720658
Abstract: The accumulation of transition metals (e.g., copper, zinc, and iron) and the dysregulation of their metabolism are a hallmark in the pathogenesis of several neurodegenerative diseases. This paper will be focused on the mechanism of neurotoxicity mediated by iron. This metal progressively accumulates in the brain both during normal aging and neurodegenerative processes. High iron concentrations in the brain have been consistently observed in Alzheimer's (AD) and Parkinson's (PD) diseases. In this connection, metalloneurobiology has become extremely important in establishing the role of iron in the onset and progression of neurodegenerative diseases. Neurons have developed several protective mechanisms against oxidative stress, among them, the activation of cellular signaling pathways. The final response will depend on the identity, intensity, and persistence of the oxidative insult. The characterization of the mechanisms mediating the effects of iron-induced increase in neuronal dysfunction and death is central to understanding the pathology of a number of neurodegenerative disorders.
Drug discovery from Chinese medicine against neurodegeneration in Alzheimer's and vascular dementia
Yuen-Shan Ho, Kwok-Fai So, Raymond Chang
Chinese Medicine , 2011, DOI: 10.1186/1749-8546-6-15
Abstract: Alzheimer's disease (AD) and vascular dementia (VaD) are the major forms of dementia. In addition, in the postmortem brains of the late stage of Parkinson's disease/Lewy body disease also find pathological hallmarks of AD [1]. Senile dementia is the progressive decline of memory and some related cognitive functions in the elderly. The global dementia population is predicted to reach 81.1 million by 2040 [2]. In 2010, the estimated prevalence of senile dementia in China is 6.0 to 7.0 million, accounting for about one-sixth of the global prevalence; the prevalence is expected to increase to 22.5 million by 2040, accounting for one-fourth of the global prevalence by that time [3]. The rapid increase in the number of dementia patients urgently demands effective prevention and treatment. Current approaches to dementia-related neurodegenerative diseases still highly rely on relieving symptoms. As some Chinese medicinal herbs have been used in treating dementia, many researchers are now turning to Chinese medicine for identifying potential neuroprotective agents or disease-modifying agent. This article reviews the strategy in the research of Chinese medicine in dementia related-neurodegenerative diseases.AD is clinically characterized by the progressive loss of memory, cognitive functions and behavioral changes. The pathogenesis of AD has been widely studied [4,5], in which beta-amyloid (Aβ) peptide and hyperphosphorylated tau protein as components of extracellular senile plaques and intracellular neurofibrillary tangles, respectively, are believed to be the targets for developing disease-modifying drugs. Current AD treatments are all symptom-relieving agents and heavily rely on the use of acetylcholinesterase (AChE) inhibitors (donepezil, rivastigmine and galantamine). AChE inhibitors slow down the degradation of the neurotransmitter acetylcholine, thereby increasing its bioavailability. Another approved AD treatment aims to reduce glutamate excitotoxicity. Memantine, the
Genomics of Dementia: APOE- and CYP2D6-Related Pharmacogenetics  [PDF]
Ramón Cacabelos,Rocío Martínez,Lucía Fernández-Novoa,Juan C. Carril,Valter Lombardi,Iván Carrera,Lola Corzo,Iván Tellado,Jerzy Leszek,Adam McKay,Masatoshi Takeda
International Journal of Alzheimer's Disease , 2012, DOI: 10.1155/2012/518901
Abstract: Dementia is a major problem of health in developed societies. Alzheimer’s disease (AD), vascular dementia, and mixed dementia account for over 90% of the most prevalent forms of dementia. Both genetic and environmental factors are determinant for the phenotypic expression of dementia. AD is a complex disorder in which many different gene clusters may be involved. Most genes screened to date belong to different proteomic and metabolomic pathways potentially affecting AD pathogenesis. The ε4 variant of the APOE gene seems to be a major risk factor for both degenerative and vascular dementia. Metabolic factors, cerebrovascular disorders, and epigenetic phenomena also contribute to neurodegeneration. Five categories of genes are mainly involved in pharmacogenomics: genes associated with disease pathogenesis, genes associated with the mechanism of action of a particular drug, genes associated with phase I and phase II metabolic reactions, genes associated with transporters, and pleiotropic genes and/or genes associated with concomitant pathologies. The APOE and CYP2D6 genes have been extensively studied in AD. The therapeutic response to conventional drugs in patients with AD is genotype specific, with CYP2D6-PMs, CYP2D6-UMs, and APOE-4/4 carriers acting as the worst responders. APOE and CYP2D6 may cooperate, as pleiotropic genes, in the metabolism of drugs and hepatic function. The introduction of pharmacogenetic procedures into AD pharmacological treatment may help to optimize therapeutics. 1. Introduction Senile dementia is a major health problem in developed countries and the primary cause of disability in the elderly. Alzheimer’s disease (AD) is the most frequent form of dementia (50–70%), followed by vascular dementia (30–40%) and mixed dementia (15–20%). These prevalent forms of age-related neurodegeneration affect over 25 million people at present, and probably over 75 million people will be at risk in the next 20–25 years worldwide. The prevalence of dementia increases exponentially from approximately 1% at 60–65 years of age to over 30–35% in people older than 80 years. It is very likely that in those patients older than 75–80 years of age most cases of dementia are mixed in nature (degenerative + vascular), whereas pure AD cases are very rare after 80 years of age. The average annual cost per person with dementia ranges from €10,000 to €40,000, depending upon disease stage and country, with a lifetime cost per patient of over €150,000. In some countries, approximately 80% of the global costs of dementia (direct + indirect costs) are assumed by the
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.