A focus on the synapse for neuroprotection in Alzheimer disease and other dementias
Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD) and are important targets for protective treatments to slow AD progression and preserve cognitive and functional abilities. Synaptic loss is the best current pathologic correlate of cognitive decline, and synap...
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| Veröffentlicht in: | Neurology 2004-10, Vol.63 (7), p.1155-1162 |
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| container_title | Neurology |
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| creator | COLEMAN, Paul FEDEROFF, Howard KURLAN, Roger |
| description | Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD) and are important targets for protective treatments to slow AD progression and preserve cognitive and functional abilities. Synaptic loss is the best current pathologic correlate of cognitive decline, and synaptic dysfunction is evident long before synapses and neurons are lost. Once synaptic function fails, even in the setting of surviving neurons, there may be little chance of effectively interfering with the disease process. This review emphasizes the importance of preserving synaptic structure and function (i.e., "synaptoprotection") in AD. Such "synaptoprotective" therapy will probably need to be administered at a critical early time point, perhaps years before onset of clinical symptoms. |
| doi_str_mv | 10.1212/01.wnl.0000140626.48118.0a |
| format | Article |
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Synaptic loss is the best current pathologic correlate of cognitive decline, and synaptic dysfunction is evident long before synapses and neurons are lost. Once synaptic function fails, even in the setting of surviving neurons, there may be little chance of effectively interfering with the disease process. This review emphasizes the importance of preserving synaptic structure and function (i.e., "synaptoprotection") in AD. Such "synaptoprotective" therapy will probably need to be administered at a critical early time point, perhaps years before onset of clinical symptoms.</description><identifier>ISSN: 0028-3878</identifier><identifier>EISSN: 1526-632X</identifier><identifier>DOI: 10.1212/01.wnl.0000140626.48118.0a</identifier><identifier>PMID: 15477531</identifier><identifier>CODEN: NEURAI</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Alzheimer Disease - pathology ; Alzheimer Disease - physiopathology ; Alzheimer Disease - therapy ; Animals ; Biological and medical sciences ; Brain - physiopathology ; Brain - ultrastructure ; Cognition - physiology ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Dementia - pathology ; Dementia - physiopathology ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. 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Synaptic loss is the best current pathologic correlate of cognitive decline, and synaptic dysfunction is evident long before synapses and neurons are lost. Once synaptic function fails, even in the setting of surviving neurons, there may be little chance of effectively interfering with the disease process. This review emphasizes the importance of preserving synaptic structure and function (i.e., "synaptoprotection") in AD. Such "synaptoprotective" therapy will probably need to be administered at a critical early time point, perhaps years before onset of clinical symptoms.</description><subject>Alzheimer Disease - pathology</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer Disease - therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - physiopathology</subject><subject>Brain - ultrastructure</subject><subject>Cognition - physiology</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Dementia - pathology</subject><subject>Dementia - physiopathology</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Neurons - physiology</subject><subject>Synapses - pathology</subject><subject>Synapses - physiology</subject><subject>Time Factors</subject><issn>0028-3878</issn><issn>1526-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFtLxDAQhYMoul7-ghRB31ozSZNMfVvEGyz6oKJvIe0mWGnTNWkR_fVGXdh5GTjznZnhEHICtAAG7JxC8em7gqaCkkomixIBsKBmi8xAMJlLzl63yYxShjlHhXtkP8b3hAumql2yB6JUSnCYkcd55oZmitngs_HNZvHLm1W0SQyZt1MYVmEYbTO2ad76bN59v9m2tyFbttGaBBq_zIbkTIrtrR9bEw_JjjNdtEfrfkCer6-eLm_zxcPN3eV8kTeCiTHHWpWsBBDSSGElo-jqSlYMecVVSamrERUYho6iMUbWDlklVYkVd3Xd1PyAnP3vTT9-TDaOum9jY7vOeDtMUUuZcOCYwIt_sAlDjME6vQptb8KXBqp_I9UU9Mv9Qm8i1X-RajpP5uP1lanu7XJjXWeYgNM1YGJjOheMb9q44SQgF6j4Dwq-f4I</recordid><startdate>20041012</startdate><enddate>20041012</enddate><creator>COLEMAN, Paul</creator><creator>FEDEROFF, Howard</creator><creator>KURLAN, Roger</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20041012</creationdate><title>A focus on the synapse for neuroprotection in Alzheimer disease and other dementias</title><author>COLEMAN, Paul ; FEDEROFF, Howard ; KURLAN, Roger</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-8b74241156a65e6208fb969283937400fb8871a28f08aaa6bf829674893fbbcb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Alzheimer Disease - pathology</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer Disease - therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain - physiopathology</topic><topic>Brain - ultrastructure</topic><topic>Cognition - physiology</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Dementia - pathology</topic><topic>Dementia - physiopathology</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Neurons - physiology</topic><topic>Synapses - pathology</topic><topic>Synapses - physiology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>COLEMAN, Paul</creatorcontrib><creatorcontrib>FEDEROFF, Howard</creatorcontrib><creatorcontrib>KURLAN, Roger</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>COLEMAN, Paul</au><au>FEDEROFF, Howard</au><au>KURLAN, Roger</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A focus on the synapse for neuroprotection in Alzheimer disease and other dementias</atitle><jtitle>Neurology</jtitle><addtitle>Neurology</addtitle><date>2004-10-12</date><risdate>2004</risdate><volume>63</volume><issue>7</issue><spage>1155</spage><epage>1162</epage><pages>1155-1162</pages><issn>0028-3878</issn><eissn>1526-632X</eissn><coden>NEURAI</coden><abstract>Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD) and are important targets for protective treatments to slow AD progression and preserve cognitive and functional abilities. Synaptic loss is the best current pathologic correlate of cognitive decline, and synaptic dysfunction is evident long before synapses and neurons are lost. Once synaptic function fails, even in the setting of surviving neurons, there may be little chance of effectively interfering with the disease process. This review emphasizes the importance of preserving synaptic structure and function (i.e., "synaptoprotection") in AD. Such "synaptoprotective" therapy will probably need to be administered at a critical early time point, perhaps years before onset of clinical symptoms.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>15477531</pmid><doi>10.1212/01.wnl.0000140626.48118.0a</doi><tpages>8</tpages></addata></record> |
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| ispartof | Neurology, 2004-10, Vol.63 (7), p.1155-1162 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection; Journals@Ovid Complete |
| subjects | Alzheimer Disease - pathology Alzheimer Disease - physiopathology Alzheimer Disease - therapy Animals Biological and medical sciences Brain - physiopathology Brain - ultrastructure Cognition - physiology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dementia - pathology Dementia - physiopathology Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Humans Medical sciences Nervous system (semeiology, syndromes) Neurology Neurons - physiology Synapses - pathology Synapses - physiology Time Factors |
| title | A focus on the synapse for neuroprotection in Alzheimer disease and other dementias |
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