Treatment with soybean lecithin-derived α-GPC (SHCog™) improves scopolamine-induced cognitive declines in mice via regulating cholinergic neurotransmission and enhancing neural plasticity in the hippocampus

Mild cognitive impairment is a diagnostic category marked by declines in memory and cognitive function that are less severe than those observed in Alzheimer's disease. Previous studies have indicated that individuals with mild cognitive impairment have an elevated risk of progressing to Alzheimer's disease. The hippocampus is well known to play pivotal roles in memory and cognitive functions. Scopolamine (Sco) disrupts cholinergic neurotransmission in the hippocampus and triggers functional declines in memory and cognition. SHCog™ is a commercially available alpha glycerophosphorylcholine (α-GPC) derived from soybean lecithin. The objective of the present study was to examine whether SHCog™ can alleviate memory and cognitive dysfunctions in a mouse model of cognitive impairments induced by Sco. In this study, C57BL/6 J mice were subjected to the passive avoidance and Morris water maze tests to investigate short-term and spatial memory functions, respectively. This study also examined cellular morphology and distribution by cresyl violet staining and investigated changes in acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) as cholinergic enzymes through immunohistochemical staining of the hippocampus. Additionally, we examined changes in postsynaptic density protein 95 (PSD-95) and brain-derived neurotrophic factor (BDNF) related to neural plasticity in the hippocampus. Treatment with SHCog™ (125 mg/kg and 250 mg/kg) brought functional recovery in short-term and spatial memory against Sco-induced memory and cognitive impairments. Changes in cellular morphology and distribution in the hippocampus were not detected following the administration of Sco and/or SHCog™. Treatment with SHCog™ reduced AChE elevated by Sco, whereas SHCog™ administration increased ChAT decreased by Sco. Furthermore, SHCog™ restored PSD-95 and BDNF in the mouse hippocampus reduced by Sco. Specifically, SHCog™ modulated cholinergic neurotransmission and enhanced neural plasticity in the hippocampus. Taken together, we suggest that SHCog™ can be a valuable ingredient in functional foods or supplements for improving memory and cognitive functions.

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Publication Details

Journal
Tissue and Cell
Published
2024-12-26
DOI
https://doi.org/10.1016/j.tice.2024.102705
Primary Topic
Neuroscience and Neuropharmacology Research
Type
article
Field-Weighted Citation Impact
0.00

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article

Treatment with soybean lecithin-derived α-GPC (SHCog™) improves scopolamine-induced cognitive declines in mice via regulating cholinergic neurotransmission and enhancing neural plasticity in the hippocampus

Ki Nam Kim, Geum Duck Park, Ga Yeon Kim, An Song et al.
Tissue and Cell
Neuroscience and Neuropharmacology Research
article

Treatment with soybean lecithin-derived α-GPC (SHCog™) improves scopolamine-induced cognitive declines in mice via regulating cholinergic neurotransmission and enhancing neural plasticity in the hippocampus

Ki Nam Kim, Geum Duck Park, Ga Yeon Kim, An Song, Tae‐Kyeong Lee, Yulong Zheng, Byong Ho Yoo
article en

Abstract

Mild cognitive impairment is a diagnostic category marked by declines in memory and cognitive function that are less severe than those observed in Alzheimer's disease. Previous studies have indicated that individuals with mild cognitive impairment have an elevated risk of progressing to Alzheimer's disease. The hippocampus is well known to play pivotal roles in memory and cognitive functions. Scopolamine (Sco) disrupts cholinergic neurotransmission in the hippocampus and triggers functional declines in memory and cognition. SHCog™ is a commercially available alpha glycerophosphorylcholine (α-GPC) derived from soybean lecithin. The objective of the present study was to examine whether SHCog™ can alleviate memory and cognitive dysfunctions in a mouse model of cognitive impairments induced by Sco. In this study, C57BL/6 J mice were subjected to the passive avoidance and Morris water maze tests to investigate short-term and spatial memory functions, respectively. This study also examined cellular morphology and distribution by cresyl violet staining and investigated changes in acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) as cholinergic enzymes through immunohistochemical staining of the hippocampus. Additionally, we examined changes in postsynaptic density protein 95 (PSD-95) and brain-derived neurotrophic factor (BDNF) related to neural plasticity in the hippocampus. Treatment with SHCog™ (125 mg/kg and 250 mg/kg) brought functional recovery in short-term and spatial memory against Sco-induced memory and cognitive impairments. Changes in cellular morphology and distribution in the hippocampus were not detected following the administration of Sco and/or SHCog™. Treatment with SHCog™ reduced AChE elevated by Sco, whereas SHCog™ administration increased ChAT decreased by Sco. Furthermore, SHCog™ restored PSD-95 and BDNF in the mouse hippocampus reduced by Sco. Specifically, SHCog™ modulated cholinergic neurotransmission and enhanced neural plasticity in the hippocampus. Taken together, we suggest that SHCog™ can be a valuable ingredient in functional foods or supplements for improving memory and cognitive functions.

Tissue and CellVol. 93
Hallym University (KR), Korea Pharma (South Korea) (KR), Yeungnam University (KR)
Ministry of Education, National Research Foundation of Korea
Zero hunger
Openalex Percentile: Top 74%
Neuroscience and Neuropharmacology Research
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