{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T16:40:39Z","timestamp":1792082439711,"version":"4.4.0"},"reference-count":106,"publisher":"Wiley","issue":"s1","license":[{"start":{"date-parts":[[2011,11,28]],"date-time":"2011-11-28T00:00:00Z","timestamp":1322438400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:sec><jats:label\/><jats:p><jats:italic>J. Neurochem.<\/jats:italic> (2012) <jats:bold>120<\/jats:bold> (Suppl. 1), 22\u201333.<\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>The prescribed drugs for treatment of cognitive deficits in Alzheimer\u2019s disease (AD) patients are regarded as symptomatic drugs. Effective disease modifying therapies are not yet prescribed in AD patients. Three major hallmarks of AD (e.g. cholinergic hypofunction, A\u03b2 and tau neuropathologies) are closely linked raising the expectation that restoring the cholinergic hypofunction to normal, in particular via selective activation of M1 muscarinic receptors, may alter the onset or progression of AD dementia. This review is focused mainly on modulation of amyloid precursor processing and A\u03b2 levels in the brain via cholinergic treatment strategies based on M1 muscarinic agonists versus other cholinergic treatments (e.g. cholinesterase inhibitors prescribed for treatment of AD, M2 antagonists and nicotinic agonists). Advantages and potential drawbacks of these treatment modalities are reviewed versus the notion that due to an elusive etiology of AD, future disease modifiers should address comprehensively most of these AD hallmarks (e.g. A\u03b2 pathology, tau and tangle pathologies, as well as the cholinergic hypofunction and cognitive impairments). This major requirement may be fulfilled with M1\u2010selective muscarinic agonists and less with other reviewed cholinergic treatments.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1471-4159.2011.07507.x","type":"journal-article","created":{"date-parts":[[2011,11,28]],"date-time":"2011-11-28T15:11:04Z","timestamp":1322493064000},"page":"22-33","source":"Crossref","is-referenced-by-count":116,"title":["Cholinergic modulation of amyloid precursor protein processing with emphasis on M1 muscarinic receptor: perspectives and challenges in treatment of Alzheimer\u2019s disease"],"prefix":"10.1111","volume":"120","author":[{"given":"Abraham","family":"Fisher","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2011,11,28]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00969687"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nn992"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0301-0082(02)00079-5"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00018-005-5597-y"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1212\/01.wnl.0000261920.03297.64"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.1006\/exnr.2000.7397"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(01)02484-2"},{"key":"e_1_2_10_9_1","first-page":"233","article-title":"Immunotoxin lesion of the cholinergic nucleus basalis causes A\u03b2 deposition: towards a physiologic animal model of Alzheimer\u2019s disease","volume":"3","author":"Beach T. 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