Novel m1 muscarinic agonists in treatment and delaying the progression of Alzheimer's disease: An unifying hypothesis
M1 selective agonists from the AF series (e.g. AF102B, AF150(S)), via m1 muscarinic receptors, activate distinct signal transductions, enhance amyloid precursors proteins secretion from transfected cells and primary cell cultures, show neurotrophic effects and are beneficial in a variety of animal m...
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| Veröffentlicht in: | Journal of physiology, Paris Paris, 1998-10, Vol.92 (5), p.337-340 |
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| container_title | Journal of physiology, Paris |
| container_volume | 92 |
| creator | Fisher, Abraham Brandeis, Rachel Haring, Rachel Eshhar, Naomi Heldman, Eliahu Karton, Yishai Eisenberg, Orli Meshulam, Haim Marciano, Daniele Bar-Ner, Nira Pittel, Zipora |
| description | M1 selective agonists from the AF series (e.g. AF102B, AF150(S)), via m1 muscarinic receptors, activate distinct signal transductions, enhance amyloid precursors proteins secretion from transfected cells and primary cell cultures, show neurotrophic effects and are beneficial in a variety of animal models for Alzheimer's disease. Such m1 agonists may be effective in the treatment and therapy of Alzheimer's disease.
Les agonistes sélectifs de type M1 appartenant à la série AF (par exemple AF102B, AF150(S)) activent de manière sélective certaines routes de transduction du signal via les récepteurs muscariniques de type m1, augmentent la sécrétion de la protéine amyloide par les cellules transfectées et les cultures primaires de cellules, produisent des effets neurotrophiques et se montrent bénéfiques pour une variété de modèles animaux de la maladie d'Alzheimer. De tels agonistes peuvent être efficaces pour traiter et guérir la maladie d'Alzheimer. |
| doi_str_mv | 10.1016/S0928-4257(99)80001-1 |
| format | Article |
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Les agonistes sélectifs de type M1 appartenant à la série AF (par exemple AF102B, AF150(S)) activent de manière sélective certaines routes de transduction du signal via les récepteurs muscariniques de type m1, augmentent la sécrétion de la protéine amyloide par les cellules transfectées et les cultures primaires de cellules, produisent des effets neurotrophiques et se montrent bénéfiques pour une variété de modèles animaux de la maladie d'Alzheimer. De tels agonistes peuvent être efficaces pour traiter et guérir la maladie d'Alzheimer.</description><identifier>ISSN: 0928-4257</identifier><identifier>EISSN: 1769-7115</identifier><identifier>DOI: 10.1016/S0928-4257(99)80001-1</identifier><identifier>PMID: 9789833</identifier><language>eng</language><publisher>France: Elsevier Ltd</publisher><subject>AF series ; Alzheimer Disease - drug therapy ; Alzheimer Disease - metabolism ; Alzheimer Disease - physiopathology ; Alzheimer's disease ; Amyloid beta-Protein Precursor - metabolism ; Animals ; Disease Progression ; Humans ; m1 agonists ; Models, Neurological ; Muscarinic Agonists - therapeutic use</subject><ispartof>Journal of physiology, Paris, 1998-10, Vol.92 (5), p.337-340</ispartof><rights>1998 Elsevier, Paris</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-a478da416e82d589f6eb99658cee923440f9ca7a780d1aa42b45f93e477d42553</citedby><cites>FETCH-LOGICAL-c426t-a478da416e82d589f6eb99658cee923440f9ca7a780d1aa42b45f93e477d42553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0928-4257(99)80001-1$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9789833$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fisher, Abraham</creatorcontrib><creatorcontrib>Brandeis, Rachel</creatorcontrib><creatorcontrib>Haring, Rachel</creatorcontrib><creatorcontrib>Eshhar, Naomi</creatorcontrib><creatorcontrib>Heldman, Eliahu</creatorcontrib><creatorcontrib>Karton, Yishai</creatorcontrib><creatorcontrib>Eisenberg, Orli</creatorcontrib><creatorcontrib>Meshulam, Haim</creatorcontrib><creatorcontrib>Marciano, Daniele</creatorcontrib><creatorcontrib>Bar-Ner, Nira</creatorcontrib><creatorcontrib>Pittel, Zipora</creatorcontrib><title>Novel m1 muscarinic agonists in treatment and delaying the progression of Alzheimer's disease: An unifying hypothesis</title><title>Journal of physiology, Paris</title><addtitle>J Physiol Paris</addtitle><description>M1 selective agonists from the AF series (e.g. AF102B, AF150(S)), via m1 muscarinic receptors, activate distinct signal transductions, enhance amyloid precursors proteins secretion from transfected cells and primary cell cultures, show neurotrophic effects and are beneficial in a variety of animal models for Alzheimer's disease. Such m1 agonists may be effective in the treatment and therapy of Alzheimer's disease.
Les agonistes sélectifs de type M1 appartenant à la série AF (par exemple AF102B, AF150(S)) activent de manière sélective certaines routes de transduction du signal via les récepteurs muscariniques de type m1, augmentent la sécrétion de la protéine amyloide par les cellules transfectées et les cultures primaires de cellules, produisent des effets neurotrophiques et se montrent bénéfiques pour une variété de modèles animaux de la maladie d'Alzheimer. De tels agonistes peuvent être efficaces pour traiter et guérir la maladie d'Alzheimer.</description><subject>AF series</subject><subject>Alzheimer Disease - drug therapy</subject><subject>Alzheimer Disease - metabolism</subject><subject>Alzheimer Disease - physiopathology</subject><subject>Alzheimer's disease</subject><subject>Amyloid beta-Protein Precursor - metabolism</subject><subject>Animals</subject><subject>Disease Progression</subject><subject>Humans</subject><subject>m1 agonists</subject><subject>Models, Neurological</subject><subject>Muscarinic Agonists - therapeutic use</subject><issn>0928-4257</issn><issn>1769-7115</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkM1P3DAQxa2qiC60fwKSTwUOATtxYpsLWiG-JEQPbc-W157sukrsrSdBWv76Zj_Etac5vPdm5v0IOePsijPeXP9kulSFKGt5ofWlYozxgn8iMy4bXUjO689k9mH5Qk4Q_2w9Qqljcqyl0qqqZmR8TW_Q0Z7TfkRnc4jBUbtMMeCANEQ6ZLBDD3GgNnrqobObEJd0WAFd57TMgBhSpKml8-59BaGHfI7UBwSLcEPnkY4xtLvMarNOUw4DfiVHre0Qvh3mKfn9cP_r7ql4-fH4fDd_KZwom6GwQipvBW9Alb5Wum1goXVTKwegy0oI1mpnpZWKeW6tKBeibnUFQko_ta6rU_J9v3d69e8IOJg-oIOusxHSiEayLRJeTcZ6b3Q5IWZozTqH3uaN4cxscZsdbrNlabQ2O9yGT7mzw4Fx0YP_SB34TvrtXoep5VuAbNAFiA58yOAG41P4z4V_f6GQ4A</recordid><startdate>19981001</startdate><enddate>19981001</enddate><creator>Fisher, Abraham</creator><creator>Brandeis, Rachel</creator><creator>Haring, Rachel</creator><creator>Eshhar, Naomi</creator><creator>Heldman, Eliahu</creator><creator>Karton, Yishai</creator><creator>Eisenberg, Orli</creator><creator>Meshulam, Haim</creator><creator>Marciano, Daniele</creator><creator>Bar-Ner, Nira</creator><creator>Pittel, Zipora</creator><general>Elsevier Ltd</general><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>19981001</creationdate><title>Novel m1 muscarinic agonists in treatment and delaying the progression of Alzheimer's disease: An unifying hypothesis</title><author>Fisher, Abraham ; Brandeis, Rachel ; Haring, Rachel ; Eshhar, Naomi ; Heldman, Eliahu ; Karton, Yishai ; Eisenberg, Orli ; Meshulam, Haim ; Marciano, Daniele ; Bar-Ner, Nira ; Pittel, Zipora</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-a478da416e82d589f6eb99658cee923440f9ca7a780d1aa42b45f93e477d42553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>AF series</topic><topic>Alzheimer Disease - drug therapy</topic><topic>Alzheimer Disease - metabolism</topic><topic>Alzheimer Disease - physiopathology</topic><topic>Alzheimer's disease</topic><topic>Amyloid beta-Protein Precursor - metabolism</topic><topic>Animals</topic><topic>Disease Progression</topic><topic>Humans</topic><topic>m1 agonists</topic><topic>Models, Neurological</topic><topic>Muscarinic Agonists - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fisher, Abraham</creatorcontrib><creatorcontrib>Brandeis, Rachel</creatorcontrib><creatorcontrib>Haring, Rachel</creatorcontrib><creatorcontrib>Eshhar, Naomi</creatorcontrib><creatorcontrib>Heldman, Eliahu</creatorcontrib><creatorcontrib>Karton, Yishai</creatorcontrib><creatorcontrib>Eisenberg, Orli</creatorcontrib><creatorcontrib>Meshulam, Haim</creatorcontrib><creatorcontrib>Marciano, Daniele</creatorcontrib><creatorcontrib>Bar-Ner, Nira</creatorcontrib><creatorcontrib>Pittel, Zipora</creatorcontrib><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>Journal of physiology, Paris</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fisher, Abraham</au><au>Brandeis, Rachel</au><au>Haring, Rachel</au><au>Eshhar, Naomi</au><au>Heldman, Eliahu</au><au>Karton, Yishai</au><au>Eisenberg, Orli</au><au>Meshulam, Haim</au><au>Marciano, Daniele</au><au>Bar-Ner, Nira</au><au>Pittel, Zipora</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Novel m1 muscarinic agonists in treatment and delaying the progression of Alzheimer's disease: An unifying hypothesis</atitle><jtitle>Journal of physiology, Paris</jtitle><addtitle>J Physiol Paris</addtitle><date>1998-10-01</date><risdate>1998</risdate><volume>92</volume><issue>5</issue><spage>337</spage><epage>340</epage><pages>337-340</pages><issn>0928-4257</issn><eissn>1769-7115</eissn><abstract>M1 selective agonists from the AF series (e.g. AF102B, AF150(S)), via m1 muscarinic receptors, activate distinct signal transductions, enhance amyloid precursors proteins secretion from transfected cells and primary cell cultures, show neurotrophic effects and are beneficial in a variety of animal models for Alzheimer's disease. Such m1 agonists may be effective in the treatment and therapy of Alzheimer's disease.
Les agonistes sélectifs de type M1 appartenant à la série AF (par exemple AF102B, AF150(S)) activent de manière sélective certaines routes de transduction du signal via les récepteurs muscariniques de type m1, augmentent la sécrétion de la protéine amyloide par les cellules transfectées et les cultures primaires de cellules, produisent des effets neurotrophiques et se montrent bénéfiques pour une variété de modèles animaux de la maladie d'Alzheimer. De tels agonistes peuvent être efficaces pour traiter et guérir la maladie d'Alzheimer.</abstract><cop>France</cop><pub>Elsevier Ltd</pub><pmid>9789833</pmid><doi>10.1016/S0928-4257(99)80001-1</doi><tpages>4</tpages></addata></record> |
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| ispartof | Journal of physiology, Paris, 1998-10, Vol.92 (5), p.337-340 |
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| language | eng |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | AF series Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - physiopathology Alzheimer's disease Amyloid beta-Protein Precursor - metabolism Animals Disease Progression Humans m1 agonists Models, Neurological Muscarinic Agonists - therapeutic use |
| title | Novel m1 muscarinic agonists in treatment and delaying the progression of Alzheimer's disease: An unifying hypothesis |
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