Centro de Biologia Molecular “Severo Ochoa”: A Center for Basic Research into Alzheimer's Disease (original) (raw)
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The beta amyloid peptide is the major component of the neuritic plaques, the characteristic lesions in Alzheimer's disease. Mutations in three genes (APP, PS-1, and PS-2) cause familial Alzheimer's disease by alteration of the rate of generation of amyloid peptide or the length of this peptide. However, in the 90% nonfamilial cases, other factors play a major pathogenetic role. These include the apolipoprotein E genotype, the "plaque-associated" proteins promoting the formation of toxic fibrillar aggregates or the chronic inflammatory responses.
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The field of neuroscience research in AD has been evolving rapidly over the last few years, and has pinpointed a number of candidate targets for molecules with crucial role in the pathophysiology of AD. Recent developments have furthermore enabled new ways of modeling the disease, while an increasing number of preclinically validated targets is currently being taken one step forward and tested in clinical trials. These recent developments are reviewed in the current Special Issues Series on "Current concepts in Alzheimer's disease research: molecules, models and translational perspectives" in a number of state-of-the-art manuscripts.
Current Drug Targets, 2003
Alzheimer's disease (AD), a progressive, degenerative disorder of the brain, is believed to be the most common cause of dementia amongst the elderly. AD is characterized by the presence of amyloid deposits and neurofibrillary tangles in the brain of afflicted individuals. AD is associated with a loss of the presynaptic markers of the cholinergic system in the brain areas related to memory and learning. AD appears to have a heterogeneous etiology with a large percentage termed sporadic AD arising from unknown causes and a smaller fraction of early onset familial AD (FAD) caused by mutations in one of several genes, such as the β-amyloid precursor protein (APP) and presenilins (PS1, PS2). These proteins along with tau, secretases, such as β-amyloid cleaving enzyme (BACE), and apolipoprotein E play important roles in the pathology of AD. On therapeutic fronts, there is significant research underway in the development of new inhibitors for BACE, PS-1 and γ-secretase as targets for treatment of AD. There is also a remarkable advancement in understanding the function of cholinesterase (ChE) in the brain and the use of ChE-inhibitors in AD. A new generation of acetyl-and butyryl cholinesterase inhibitors is being studied and tested in human clinical trials for AD. The development of vaccination strategies, anti-inflammatory agents, cholesterol-lowering agents, anti-oxidants and hormone therapy are examples of new approaches for treating or slowing the progression of AD. In addition, nutritional, genetic and environmental factors highlight more effective preventive strategies for AD. Developments of early diagnostic tools and of quantitative markers are critical to better follow the course of the disease and to evaluate different therapeutic strategies. In this review, we attempt to critically examine recent trends in AD research from molecular, genetic to clinical areas. We discuss various neurobiological mechanisms that provide the basis of new targets for AD drug development. All these current research efforts should lead to a deeper understanding of the pathobiochemical processes that occur in the AD brain in order to effectively diagnose and prevent their occurrence.
Molecular Mechanism of Promotion, Progression and Possible Therapies of Alzheimer's Disease
2022
Objective: Alzheimer’s disease (AD) is the common neurodegenerative disorder in the world, and intracellular neurofibrillary tangles and extracellular amyloid-beta (Aβ) protein deposits correspond to the most important pathological hallmarks of the disease. The current study is particularly concerned with molecular mechanisms underneath the promotion of AD. There is no cure reported for AD, although the therapeutic treatments mainly improve the symptoms of the disease. Consequently, an early and appropriate diagnosis is crucial to slow the evolution of the disease. The purpose of Tau and Aβ levels in the blood and cerebrospinal fluid (CSF) are generally used for the diagnosis of AD. Several medical equipment are also used to verify the diagnosis including the medical history, mental status tests, and evaluations of the brain construction with neuroimaging techniques. Molecular genetics is proved to be a precious tool to recognize the molecular origin of AD. Although several commerci...
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Gazi University Journal of Science, 2012
The prevalence of Alzheimer's disease ranges from 3-11% in persons over ages 65 years. It is a significant problem about aging. It is reported that most of 70 to50% of demantias is Alzheimer`s disease in Western Europe and the United States according to Japan moreover Russia researchers have been reported that there is more multi infarct demantias. In addition, the incidence of the disease and epidemiological studies have not still determine yet in Turkey.A great deal of research has been conducted recently; and the knowledge of the clinical characteristics, neuropathology, genetics, and possible treatments has accumulated. In this review, these improvements will be summarised.
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Translational Neuroscience, 2014
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Background and objective: Alzheimer's disease (AD) - the main cause of dementia - is characterized by the presence of neuritic plaques containing the amyloid- peptide (A) and an intraneuronal accumulation of tubule-associated protein called tau. The current and future therapeutic strategies for AD will be discussed. Currently available treatment used in AD is based on acetylcholinesterase inhibitors, since in the
Neurobiology of Disease, 2020
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