{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:45:13Z","timestamp":1787024713024,"version":"build-2736575974"},"reference-count":218,"publisher":"Bentham Science Publishers Ltd.","issue":"2","content-domain":{"domain":["eurekaselect.com"],"crossmark-restriction":true},"short-container-title":["CNSNDDT"],"published-print":{"date-parts":[[2023,2]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract:<\/jats:title>\n                    <jats:p>Alzheimer\u2019s disease (AD) is the most prevalent form of dementia among geriatrics. It is a\nprogressive, degenerative neurologic disorder that causes memory and cognition loss. The accumulation\nof amyloid fibrils and neurofibrillary tangles in the brain of AD patients is a distinguishing feature\nof the disease. Therefore, most of the current therapeutic goals are targeting inhibition of beta-amyloid\nsynthesis and aggregation as well as tau phosphorylation and aggregation. There is also a loss of the\ncholinergic neurons in the basal forebrain, and first-generation therapeutic agents were primarily focused\non compensating for this loss of neurons. However, cholinesterase inhibitors can only alleviate\ncognitive symptoms of AD and cannot reduce the progression of the disease. Understanding the molecular\nand cellular changes associated with AD pathology has advanced significantly in recent decades.\nThe etiology of AD is complex, with a substantial portion of sporadic AD emerging from unknown\nreasons and a lesser proportion of early-onset familial AD (FAD) caused by a mutation in several\ngenes, such as the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2)\ngenes. Hence, efforts are being made to discover novel strategies for these targets for AD therapy. A\nnew generation of AChE and BChE inhibitors is currently being explored and evaluated in human\nclinical trials for AD symptomatic treatment. Other approaches for slowing the progression of AD include\nserotonergic modulation, H3 receptor antagonism, phosphodiesterase, COX-2, and MAO-B inhibition.\nThe present review provides an insight into the possible therapeutic strategies and their molecular\nmechanisms, enlightening the perception of classical and future treatment approaches.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2174\/1871527321666220401124719","type":"journal-article","created":{"date-parts":[[2022,4,3]],"date-time":"2022-04-03T14:09:36Z","timestamp":1648994976000},"page":"255-275","update-policy":"https:\/\/doi.org\/10.2174\/bsp_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Current Drug Targets in Alzheimer\u2019s Associated Memory Impairment: A\nComprehensive Review"],"prefix":"10.2174","volume":"22","author":[{"given":"Chandrashekar","family":"K.S","sequence":"first","affiliation":[{"name":"Department of Pharmacognosy, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education,\nManipal, Karnataka-576104, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Mathew","sequence":"additional","affiliation":[{"name":"Department of Pharmacognosy, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education,\nManipal, Karnataka-576104, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vignesh","family":"Balaji E","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Manipal College of Pharmaceutical Sciences,\nManipal Academy of Higher Education, Manipal, Karnataka-576104, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sreedhara Ranganath K.","family":"Pai","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal, Karnataka-576104, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anoop","family":"Kishore","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal, Karnataka-576104, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vasudev","family":"Pai","sequence":"additional","affiliation":[{"name":"Department of Pharmacognosy, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education,\nManipal, Karnataka-576104, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ramadevi","family":"Pemmireddy","sequence":"additional","affiliation":[{"name":"Department of Pharmacognosy, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education,\nManipal, Karnataka-576104, India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"965","reference":[{"key":"ref=1","doi-asserted-by":"publisher","first-page":"91","DOI":"10.31887\/DCNS.2000.2.2\/asschachter","volume":"2","author":"Schachter A.S.","year":"2000","unstructured":"Schachter A.S.; Davis K.L.; Alzheimer\u2019s disease. 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