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100 Years and Counting: Prospects for Defeating Alzheimer's Disease

This week marks a century since the first description of Alzheimer's disease (AD). Despite approval of several drugs for AD, the disease continues to rob millions of their memories and their lives. Fortunately, many new therapies directly targeting the mechanisms underlying AD are now in the pi...

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Published in:Science (American Association for the Advancement of Science) 2006-11, Vol.314 (5800), p.781-784
Main Authors: Roberson, Erik D, Mucke, Lennart
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Language:English
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description This week marks a century since the first description of Alzheimer's disease (AD). Despite approval of several drugs for AD, the disease continues to rob millions of their memories and their lives. Fortunately, many new therapies directly targeting the mechanisms underlying AD are now in the pipeline. Among the investigative AD therapies in clinical trials are several strategies to block pathogenic amyloid-β peptides and to rescue vulnerable neurons from degeneration. Complementary but less mature strategies aim to prevent the copathogenic effects of apolipoprotein E and the microtubule-associated protein tau. New insights into selective neuronal vulnerability and the link between aging and AD may provide additional entry points for therapeutic interventions. The predicted increase in AD cases over the next few decades makes the development of better treatments a matter of utmost importance and urgency.
doi_str_mv 10.1126/science.1132813
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Despite approval of several drugs for AD, the disease continues to rob millions of their memories and their lives. Fortunately, many new therapies directly targeting the mechanisms underlying AD are now in the pipeline. Among the investigative AD therapies in clinical trials are several strategies to block pathogenic amyloid-β peptides and to rescue vulnerable neurons from degeneration. Complementary but less mature strategies aim to prevent the copathogenic effects of apolipoprotein E and the microtubule-associated protein tau. New insights into selective neuronal vulnerability and the link between aging and AD may provide additional entry points for therapeutic interventions. The predicted increase in AD cases over the next few decades makes the development of better treatments a matter of utmost importance and urgency.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.1132813</identifier><identifier>PMID: 17082448</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Association for the Advancement of Science</publisher><subject>Adult and adolescent clinical studies ; Alzheimer Disease - pathology ; Alzheimer Disease - physiopathology ; Alzheimer Disease - therapy ; Alzheimer's disease ; Alzheimers disease ; Amyloid beta-Peptides - immunology ; Amyloid beta-Peptides - metabolism ; Animals ; Biological and medical sciences ; Brain ; Cholinesterase inhibitors ; Clinical trials ; Clinical Trials as Topic ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Enzyme Inhibitors - therapeutic use ; Enzymes ; History of medicine ; Humans ; Immunization ; Immunization, Passive ; Medical research ; Medical sciences ; Medical treatment ; Nervous system diseases ; Neurology ; Neurons ; Neuroscience ; Nootropic Agents - therapeutic use ; Organic mental disorders. Neuropsychology ; Peptides ; Pharmacology ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. 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Despite approval of several drugs for AD, the disease continues to rob millions of their memories and their lives. Fortunately, many new therapies directly targeting the mechanisms underlying AD are now in the pipeline. Among the investigative AD therapies in clinical trials are several strategies to block pathogenic amyloid-β peptides and to rescue vulnerable neurons from degeneration. Complementary but less mature strategies aim to prevent the copathogenic effects of apolipoprotein E and the microtubule-associated protein tau. New insights into selective neuronal vulnerability and the link between aging and AD may provide additional entry points for therapeutic interventions. The predicted increase in AD cases over the next few decades makes the development of better treatments a matter of utmost importance and urgency.</description><subject>Adult and adolescent clinical studies</subject><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer Disease - therapy</subject><subject>Alzheimer's disease</subject><subject>Alzheimers disease</subject><subject>Amyloid beta-Peptides - immunology</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Cholinesterase inhibitors</subject><subject>Clinical trials</subject><subject>Clinical Trials as Topic</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Enzymes</subject><subject>History of medicine</subject><subject>Humans</subject><subject>Immunization</subject><subject>Immunization, Passive</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Medical treatment</subject><subject>Nervous system diseases</subject><subject>Neurology</subject><subject>Neurons</subject><subject>Neuroscience</subject><subject>Nootropic Agents - therapeutic use</subject><subject>Organic mental disorders. Neuropsychology</subject><subject>Peptides</subject><subject>Pharmacology</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. 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Despite approval of several drugs for AD, the disease continues to rob millions of their memories and their lives. Fortunately, many new therapies directly targeting the mechanisms underlying AD are now in the pipeline. Among the investigative AD therapies in clinical trials are several strategies to block pathogenic amyloid-β peptides and to rescue vulnerable neurons from degeneration. Complementary but less mature strategies aim to prevent the copathogenic effects of apolipoprotein E and the microtubule-associated protein tau. New insights into selective neuronal vulnerability and the link between aging and AD may provide additional entry points for therapeutic interventions. 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subjects Adult and adolescent clinical studies
Alzheimer Disease - pathology
Alzheimer Disease - physiopathology
Alzheimer Disease - therapy
Alzheimer's disease
Alzheimers disease
Amyloid beta-Peptides - immunology
Amyloid beta-Peptides - metabolism
Animals
Biological and medical sciences
Brain
Cholinesterase inhibitors
Clinical trials
Clinical Trials as Topic
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Enzyme Inhibitors - therapeutic use
Enzymes
History of medicine
Humans
Immunization
Immunization, Passive
Medical research
Medical sciences
Medical treatment
Nervous system diseases
Neurology
Neurons
Neuroscience
Nootropic Agents - therapeutic use
Organic mental disorders. Neuropsychology
Peptides
Pharmacology
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Reviews
Vaccination
title 100 Years and Counting: Prospects for Defeating Alzheimer's Disease
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