{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T12:18:59Z","timestamp":1788437939007,"version":"build-2803163510"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>Abstract:<\/jats:title>\n                  <jats:p>Parkinson\u2019s disease (PD) is an incurable progressive neurodegenerative condition, which is characterized by a selective loss of dopaminergic neurons in the substantia nigra and subsequent development of motor impairment along with a non-motoric syndrome. It has a multifactorial etiopathogenesis, including oxidative stress, mitochondrial failure, lasting neuroinflammation, and \u03b1-synuclein aggregation. Interestingly, acetoside and arbutin are naturally occurring phenolic glycosides that have gained increased attention in recent times due to their strong antioxidant, anti-inflammatory, and neuroprotective capabilities. These agents have been empirically demonstrated to reduce reactive oxygen species, energize endogenous antioxidant defenses such as superoxide dismutase, catalase (CAT), glutathione, maintain mitochondrial integrity, and salvage adenosine triphosphate (ATP) generation. Furthermore, they inhibit pro-inflammatory mediators such as tumor necrosis factor-alpha (TNF-\u03b1), prevent the activation of caspase-3 and lipid peroxidation, regulate AMP-activated protein kinase and p62 signaling pathways, and alleviate the loss of dopaminergic neurons, which results in improved motor performance. Computational docking reports have revealed positive results between arbutin, acetoside, and key targets of PD (e.g., acetylcholinesterase [AChE], TNF-\u03b1, caspase-3, CAT, dopamine-associated proteins, and \u03b1-synuclein). Arbutin showed binding energies of \u2212 7.6 kcal\/mol (AChE), \u22127.0 kcal\/mol (caspase-3), \u22129.0 kcal\/mol (CAT), \u22128.8 kcal\/mol (TNF-\u03b1), and \u2212 7.0 kcal\/mol (dopaminergic targets). In contrast, acetoside showed stronger interactions with corresponding targets, exhibiting binding energies of \u2212 8.7 kcal\/mol, \u22128.9 kcal\/mol, \u22129.7 kcal\/mol, and \u2212 8.9 kcal\/mol. Collectively, these findings highlight phenolic glycosides as promising multitarget neuroprotective candidates for PD.<\/jats:p>","DOI":"10.4103\/ijp.ijp_68_26","type":"journal-article","created":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T13:00:40Z","timestamp":1788354040000},"page":"495-504","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":0,"title":["Role of arbutin and acetoside against Parkinson\u2019s disease"],"prefix":"10.4103","volume":"58","author":[{"given":"Anish","family":"Singh","sequence":"first","affiliation":[{"name":"University Institute of Pharma Sciences, Chandigarh University, Mohali, Punjab, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diksha","family":"Dalal","sequence":"additional","affiliation":[{"name":"School of Pharmaceutical Sciences, CGC University, Mohali, Punjab, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lovedeep","family":"Singh","sequence":"additional","affiliation":[{"name":"University Institute of Pharma Sciences, Chandigarh University, Mohali, Punjab, India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2026,9,2]]},"reference":[{"key":"R1-20260903","doi-asserted-by":"crossref","first-page":"896","DOI":"10.1016\/S0140-6736(14)61393-3","article-title":"Parkinson\u2019s disease","volume":"386","author":"Kalia","year":"2015","journal-title":"Lancet"},{"key":"R2-20260903","doi-asserted-by":"crossref","first-page":"17013","DOI":"10.1038\/nrdp.2017.13","article-title":"Parkinson disease","volume":"3","author":"Poewe","year":"2017","journal-title":"Nat Rev Dis Primers"},{"key":"R3-20260903","doi-asserted-by":"crossref","first-page":"235","DOI":"10.1016\/S1474-4422(06)70373-8","article-title":"Non-motor symptoms of Parkinson\u2019s disease: Diagnosis and management","volume":"5","author":"Chaudhuri","year":"2006","journal-title":"Lancet Neurol"},{"key":"R4-20260903","doi-asserted-by":"crossref","first-page":"839","DOI":"10.1038\/42166","article-title":"Alpha-synuclein in Lewy bodies","volume":"388","author":"Spillantini","year":"1997","journal-title":"Nature"},{"key":"R5-20260903","doi-asserted-by":"crossref","first-page":"132","DOI":"10.1016\/j.freeradbiomed.2013.01.018","article-title":"Parkinson disease: From pathology to molecular disease mechanisms","volume":"62","author":"Dexter","year":"2013","journal-title":"Free Radic Biol Med"},{"key":"R6-20260903","doi-asserted-by":"crossref","first-page":"101","DOI":"10.1038\/nrn.2016.178","article-title":"Selective neuronal vulnerability in Parkinson disease","volume":"18","author":"Surmeier","year":"2017","journal-title":"Nat Rev Neurosci"},{"issue":"Suppl 1","key":"R7-20260903","doi-asserted-by":"crossref","first-page":"325","DOI":"10.1111\/jnc.13750","article-title":"Current and experimental treatments of Parkinson disease: A guide for neuroscientists","volume":"139","author":"Oertel","year":"2016","journal-title":"J Neurochem"},{"issue":"(1 Suppl)","key":"R8-20260903","doi-asserted-by":"crossref","first-page":"230S","DOI":"10.1093\/ajcn\/81.1.230S","article-title":"Bioavailability and bioefficacy of polyphenols in humans. 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