共查询到20条相似文献,搜索用时 0 毫秒
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《Current biology : CB》2014,24(4):R157-R159
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《基因组蛋白质组与生物信息学报(英文版)》2016,(5):289-297
Alzheimer’s disease (AD) remains to be a grand challenge for the international commu-nity despite over a century of exploration. A key factor likely accounting for such a situation is the vast heterogeneity in the disease etiology, which involves very complex and divergent pathways. Therefore, intervention strategies shall be tailored for subgroups of AD patients. Both demographic and in-depth information is needed for patient stratification. The demographic information includes primarily APOE genotype, age, gender, education, environmental exposure, life style, and medical history, whereas in-depth information stems from genome sequencing, brain imaging, peripheral biomarkers, and even functional assays on neurons derived from patient-specific induced pluripo-tent cells (iPSCs). Comprehensive information collection, better understanding of the disease mech-anisms, and diversified strategies of drug development would help with more effective intervention in the foreseeable future. 相似文献
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Stephen B. Pyecroft Anne-Maree Pearse Richmond Loh Kate Swift Kathy Belov Nolan Fox Erin Noonan Dane Hayes Alex Hyatt Lingfa Wang David Boyle Jeff Church Debra Middleton Robert Moore 《EcoHealth》2007,4(3):346-351
In the mid 1990s an emerging disease characterised by the development of proliferative lesions around the face of Tasmanian
devils (Sarcophilus harrisii) was observed. A multi-disciplinary approach was adopted to define the condition. Histopathological and transmission electron
microscopic examination combined with immunohistochemistry help define Devil Facial Tumour Disease (DFTD) as a neoplastic
condition of cells of neuroendocrine origin. Cytogenetic analysis of neoplastic tissue revealed it to be markedly different
from normal devil tissue and having a consistent karyotype across all tumours examined. Combined with evidence for Major histocompatability
(MHC) gene analysis there is significant evidence to confirm the tumour is a transmissible neoplasm. 相似文献
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Parisa Farzanehfar 《Neurochemical research》2016,41(12):3161-3170
The motor symptoms of Parkinson’s disease (PD) are caused by degeneration of dopamine (DA) neurons in the substantia nigra pars compacta (SNc) of midbrain. Given the fact that current treatment options are mostly symptomatic and based on increasing DA level in the nigrostriatal system, it is generally believed the most effective and long-lasting treatment for PD motor symptoms will be replacing SNc DA cells, either by endogenous repair (i.e. neurogenesis) or cell transplantation. While cell transplantation is hindered by failure of acquisition and maintenance of the DA phenotype by transplanted cells, hope rests upon non-invasive cell replacement therapy (CRT) with endogenous neural stem cells, which have the potential to give rise to new neurons including DA neurons. Understanding underlying mechanisms and signalling pathways of neurogenesis in the adult brain could shed light on obstacles to achieve effective CRTs and better treatments for PD. This paper first reviews different therapeutic strategies in context of PD along with their advantages and disadvantages followed by an extensive review of adult neurogenesis. 相似文献
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Shields R 《PLoS biology》2011,9(1):e1001009
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Kaur Dapinder Behl Tapan Sehgal Aayush Singh Sukhbir Sharma Neelam Bungau Simona 《Neurochemical research》2021,46(11):2832-2851
Neurochemical Research - Alzheimer's disease (AD) is one of the most prevailing neurodegenerative disorders of elderly humans associated with cognitive damage. Biochemical, epigenetic, and... 相似文献
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Bo Su Xinglong Wang David Bonda Gorge Perry Mark Smith Xiongwei Zhu 《Molecular neurobiology》2010,41(2-3):87-96
Mitochondria are dynamic organelles that undergo continuous fission and fusion, which could affect all aspects of mitochondrial function. Mitochondrial dysfunction has been well documented in Alzheimer’s disease (AD). In the past few years, emerging evidence indicates that an imbalance of mitochondrial dynamics is involved in the pathogenesis of AD. In this review, we discuss in detail the abnormal mitochondrial dynamics in AD and how such abnormal dynamics may impact mitochondrial and neuronal function and contribute to the course of disease. Based on this discussion, we propose that mitochondrial dynamics could be a potential therapeutic target for AD. 相似文献
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Charles F. Macquibban 《BMJ (Clinical research ed.)》1879,1(954):543-544
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Disease modifying therapy for AD?1 总被引:10,自引:0,他引:10
Golde TE 《Journal of neurochemistry》2006,99(3):689-707
Alzheimer's disease (AD) is the most common form of dementia in industrialized nations. If more effective therapies are not developed that either prevent AD or block progression of the disease in its very early stages, the economic and societal cost of caring for AD patients will be devastating. Only two types of drugs are currently approved for the treatment of AD: inhibitors of acetyl cholinesterase, which symptomatically enhance cognitive state to some degree but are not disease modifying; and the adamantane derivative, memantine. Memantine preferentially blocks excessive NMDA receptor activity without disrupting normal receptor activity and is thought to be a neuroprotective agent that blocks excitotoxicty. Memantine therefore may have a potentially disease modifying effect in multiple neurodegenerative conditions. An improved understanding of the pathogeneses of AD has now led to the identification of numerous therapeutic targets designed to alter amyloid beta protein (Abeta) or tau accumulation. Therapies that alter Abeta and tau through these various targets are likely to have significant disease modifying effects. Many of these targets have been validated in proof of concept studies in preclinical animal models, and some potentially disease modifying therapies targeting Abeta or tau are being tested in the clinic. This review will highlight both the promise of and the obstacles to developing such disease modifying AD therapies. 相似文献
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