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In the past two decades there have been significant advances made in understanding the cellular and molecular alterations that occur with brain ageing, as well as with our understanding of age-related brain diseases. Ageing is associated with a mid-life decline in many cognitive domains (eg. Attention, working memory, episodic memory) that progresses with advancing age and which may be potentiated by a variety of diseases. However, despite the breadth of attempts to explain it, the underlying basis for age-related memory impairment remains poorly understood. Both normal and “pathological” ageing (as in age-related neurodegenerative disorders such as Alzheimer’s disease) may be associated with overlapping and increased levels of “abnormal” pathology, and this may be a potential mediator of cognitive decline in both populations. An emerging hypothesis in this field is that metal ion dys/homeostasis may represent a primary unifying mechanism to explain age- and disease-associated memory impairment – either indirectly via an effect on disease pathogenesis, or by a direct effect on signaling pathways relevant to learning and memory. There remains a concerted worldwide effort to deliver an effective therapeutic treatment for cognitive decline associated with ageing and/or disease, which is currently an unmet need. There have been numerous clinical trials conducted specifically testing drugs to prevent cognitive decline and progression to dementia, but to date the results have been less than impressive, highlighting the urgent need for a greater understanding of the neurobiological basis of memory impairment in ageing and disease which can then drive the search for effective therapeutics.
Down Syndrome --- Amyotrophic Lateral Sclerosis --- Parkinson's disease --- aluminium --- Iron --- TBI --- Cognition --- Copper --- Alzheimer's disease --- Zinc
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The Golgi apparatus is a central organelle that lies at the heart of the secretory pathway. It ensures post-translational protein modifications such as glycosylation and cleavage as well as protein sorting to neuronal axons and dendrites. Structural and functional alterations of the Golgi apparatus (fragmentation and atrophy), which are collectively termed Golgi pathology, are now recognized as a constant feature of many neuro-degenerative diseases. However, the molecular mechanisms underlying these changes and their precise relevance to neurodegeneration have not yet been completely elucidated. This eBook contains 13 reviews that address the molecular mechanisms of Golgi pathology in Parkinson and Alzheimer diseases, amyotrophic lateral sclerosis (ALS) and spinal muscular atrophies, and discuss their potential relevance to the pathological loss of neuronal cell bodies, axons and synapses.
Neurodegenerative Diseases --- Intracellular membrane traffic --- Amyotrophic Lateral Sclerosis --- signaling --- Golgi fragmentation --- Microtubules --- Cell Death --- Tethers --- molecular motors --- vesicles
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The Golgi apparatus is a central organelle that lies at the heart of the secretory pathway. It ensures post-translational protein modifications such as glycosylation and cleavage as well as protein sorting to neuronal axons and dendrites. Structural and functional alterations of the Golgi apparatus (fragmentation and atrophy), which are collectively termed Golgi pathology, are now recognized as a constant feature of many neuro-degenerative diseases. However, the molecular mechanisms underlying these changes and their precise relevance to neurodegeneration have not yet been completely elucidated. This eBook contains 13 reviews that address the molecular mechanisms of Golgi pathology in Parkinson and Alzheimer diseases, amyotrophic lateral sclerosis (ALS) and spinal muscular atrophies, and discuss their potential relevance to the pathological loss of neuronal cell bodies, axons and synapses.
Neurodegenerative Diseases --- Intracellular membrane traffic --- Amyotrophic Lateral Sclerosis --- signaling --- Golgi fragmentation --- Microtubules --- Cell Death --- Tethers --- molecular motors --- vesicles
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In the past two decades there have been significant advances made in understanding the cellular and molecular alterations that occur with brain ageing, as well as with our understanding of age-related brain diseases. Ageing is associated with a mid-life decline in many cognitive domains (eg. Attention, working memory, episodic memory) that progresses with advancing age and which may be potentiated by a variety of diseases. However, despite the breadth of attempts to explain it, the underlying basis for age-related memory impairment remains poorly understood. Both normal and “pathological” ageing (as in age-related neurodegenerative disorders such as Alzheimer’s disease) may be associated with overlapping and increased levels of “abnormal” pathology, and this may be a potential mediator of cognitive decline in both populations. An emerging hypothesis in this field is that metal ion dys/homeostasis may represent a primary unifying mechanism to explain age- and disease-associated memory impairment – either indirectly via an effect on disease pathogenesis, or by a direct effect on signaling pathways relevant to learning and memory. There remains a concerted worldwide effort to deliver an effective therapeutic treatment for cognitive decline associated with ageing and/or disease, which is currently an unmet need. There have been numerous clinical trials conducted specifically testing drugs to prevent cognitive decline and progression to dementia, but to date the results have been less than impressive, highlighting the urgent need for a greater understanding of the neurobiological basis of memory impairment in ageing and disease which can then drive the search for effective therapeutics.
Down Syndrome --- Amyotrophic Lateral Sclerosis --- Parkinson's disease --- aluminium --- Iron --- TBI --- Cognition --- Copper --- Alzheimer's disease --- Zinc
Choose an application
In the past two decades there have been significant advances made in understanding the cellular and molecular alterations that occur with brain ageing, as well as with our understanding of age-related brain diseases. Ageing is associated with a mid-life decline in many cognitive domains (eg. Attention, working memory, episodic memory) that progresses with advancing age and which may be potentiated by a variety of diseases. However, despite the breadth of attempts to explain it, the underlying basis for age-related memory impairment remains poorly understood. Both normal and “pathological” ageing (as in age-related neurodegenerative disorders such as Alzheimer’s disease) may be associated with overlapping and increased levels of “abnormal” pathology, and this may be a potential mediator of cognitive decline in both populations. An emerging hypothesis in this field is that metal ion dys/homeostasis may represent a primary unifying mechanism to explain age- and disease-associated memory impairment – either indirectly via an effect on disease pathogenesis, or by a direct effect on signaling pathways relevant to learning and memory. There remains a concerted worldwide effort to deliver an effective therapeutic treatment for cognitive decline associated with ageing and/or disease, which is currently an unmet need. There have been numerous clinical trials conducted specifically testing drugs to prevent cognitive decline and progression to dementia, but to date the results have been less than impressive, highlighting the urgent need for a greater understanding of the neurobiological basis of memory impairment in ageing and disease which can then drive the search for effective therapeutics.
Down Syndrome --- Amyotrophic Lateral Sclerosis --- Parkinson's disease --- aluminium --- Iron --- TBI --- Cognition --- Copper --- Alzheimer's disease --- Zinc
Choose an application
The Golgi apparatus is a central organelle that lies at the heart of the secretory pathway. It ensures post-translational protein modifications such as glycosylation and cleavage as well as protein sorting to neuronal axons and dendrites. Structural and functional alterations of the Golgi apparatus (fragmentation and atrophy), which are collectively termed Golgi pathology, are now recognized as a constant feature of many neuro-degenerative diseases. However, the molecular mechanisms underlying these changes and their precise relevance to neurodegeneration have not yet been completely elucidated. This eBook contains 13 reviews that address the molecular mechanisms of Golgi pathology in Parkinson and Alzheimer diseases, amyotrophic lateral sclerosis (ALS) and spinal muscular atrophies, and discuss their potential relevance to the pathological loss of neuronal cell bodies, axons and synapses.
Neurodegenerative Diseases --- Intracellular membrane traffic --- Amyotrophic Lateral Sclerosis --- signaling --- Golgi fragmentation --- Microtubules --- Cell Death --- Tethers --- molecular motors --- vesicles
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This book contains selected peer-reviewed chapters which cover updated information on ALS written by international researchers. Update on Amyotrophic Lateral Sclerosis is comprised of 13 chapters from some of the world's top central nervous system researchers and neurologists to provide a timely review of the most recent developments in ALS, covering historic aspects, experimental animal models, genetics, pathogenesis, clinical aspects and imagenology among others. Contributors from Belgium, France, Japan, India, Italy, Mexico, Russia, South Africa, and Switzerland have collaborated enthusiastically and efficiently, dedicating their time to create this reader-friendly yet comprehensive work which includes many explanatory figures, tables and photos to enhance legibility and make the book clinically useful. We are looking forward with confidence and pride in the remarkable role that this book will play for a new vision and mission.
Amyotrophic lateral sclerosis. --- ALS (Disease) --- Gehrig's disease --- Lateral sclerosis --- Lou Gehrig's disease --- Motor neurone disease --- Sclerosis, Amyotrophic lateral --- Motor neurons --- Neuromuscular diseases --- Diseases --- Medicine --- Neurology --- Mental and Behavioural Disorders and Diseases of the Nervous System --- Health Sciences
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Amyotrophic lateral sclerosis is a fatal and progressive disease, characterized by progressive muscles weakness, with consequent loss of physical capacities. Patients become relentlessly immobile and, in the late stages of the disease, develop a locked-in state in which only residual muscular movement is possible, but the intellect and the personality usually remain unimpaired. At now, there is no cure for ALS. The psychological impact of the disease is huge, on both patients and caregivers. Aim of the present Research Topic is to collect new evidence about quality of life, depression, anxiety, pain, spiritual and existential issues, hope and hopelessness in the ALS field, with attention to both patients and their caregivers. Emphasis will be provided to the investigation of psychological support and the possible role of psychologists in this challenging field.
Amyotrophic lateral sclerosis --- Quality of life. --- Clinical psychology. --- Psychological aspects. --- Psychiatry --- Psychology, Applied --- Psychological tests --- Life, Quality of --- Economic history --- Human ecology --- Life --- Social history --- Basic needs --- Human comfort --- Social accounting --- Work-life balance --- ALS (Disease) --- Gehrig's disease --- Lateral sclerosis --- Lou Gehrig's disease --- Motor neurone disease --- Sclerosis, Amyotrophic lateral --- Motor neurons --- Neuromuscular diseases --- Diseases --- clinical psychology --- Amyotrophic Lateral Sclerosis --- medical psychology --- Quality of Life --- Health Psychology --- Chronic disorders
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