Plexiform Ameloblastoma with Acanthomatous Changes: A Rare Case Report.

UNLABELLED: Cognitive impairment is a major feature of neurodegenerative disorders and is associated with cholinergic dysfunction, oxidative stress, neuroinflammation, and impaired neuroplasticity. Acemannan, a bioactive acetylated β-(1→4)-linked polymannan derived from Aloe vera (Aloe barbadensis Mill.), exhibits antioxidant and anti-inflammatory properties, suggesting potential neuroprotective effects. This study investigated the neuroprotective effect of acemannan against scopolamine-induced cognitive impairments in Wistar rats. Morris Water Maze, Y-maze, Novel Object Recognition, and rotarod tests were used to assess behavioral activity. Upon completion of the treatment, biochemical analysis such as neurotransmitters (Ach, GABA, DA, 5HT, Glu), cholinergic markers (AChE, ChAT), oxidative stress indicators (MDA, NO) antioxidant enzymes (SOD, CAT, GSH), inflammatory cytokines (IL-1β, IL-6, TNF-α), and apoptotic/neuroplasticity markers (caspase-3, BDNF, CREB, SIRT1, PGC-1α) and Histopathology were also performed. Additionally, molecular docking was conducted using GlycoTorch Vina, a carbohydrate-specific molecular docking tool, to investigate the binding interactions and affinity of acemannan with selected protein targets. The in vitro analysis showed an AChE inhibitory effect. Administration of scopolamine impaired cognitive and motor activity, as indicated by increased oxidative and inflammatory markers and disrupted neurotransmitter levels. However, acemannan treatment reversed these abnormal effects and improved behavioral performance. Additionally, it restored the levels of neurotransmitters (Ach, GABA, DA, 5HT, Glu), cholinergic enzymes (AChE, ChAT), reduced oxidative stress markers (MDA, NO), and inflammatory markers (IL-1β, IL-6, TNF-α), and increased antioxidant enzymes (SOD, CAT, GSH), decreased Caspase-3,enhanced neuroplasticity markers (BDNF, CREB, SIRT1, PGC-1α). Acemannan showed substantial neuroprotection, with mostly normal pyramidal cells. Molecular docking revealed that acemannan showed favorable binding affinity with CHRM1 (5CXV, - 6.1 to - 5.4 kcal/mol), followed by BDNF (1B8M, - 4.8 to - 4.4 kcal/mol), and TNF-α (7JRA, - 4.3 to - 3.0 kcal/mol). Overall, acemannan attenuated scopolamine-induced cognitive impairment through multiple neuroprotective mechanisms, supporting its potential as a neuroprotective candidate for cognitive dysfunction associated with neurodegenerative disorders in this model of rats.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at https://doi.org/10.1007/s13205-026-05068-4.