Glucosamine Enhancement of BDNF Expression and Animal Cognitive Function

Chou, Lien Yu; Chao, Yu Ming; Peng, Yen Chun; Lin, Hui Ching; Wu, Yuh Lin

doi:10.3390/molecules25163667

Cited by 13 publications

(15 citation statements)

References 34 publications

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“…Neurotrophic factors play a crucial role in neurogenesis ( Agrimi et al, 2019 ). It has been found that BDNF is an important neurotrophic factor and its signaling inhibits autophagy in an adult brain by transcriptionally downregulating key ( Patterson, 2015 ; Chou et al, 2020 ) components of the autophagy machinery and that genetic ablation of BDNF in the nervous system leads to uncontrolled increases in autophagy in the adult brain and is associated with severe synaptic defect ( Nikoletopoulou et al, 2017 ). Decreased levels of BDNF in the hippocampus can aggravate cognitive impairment.…”

Section: Discussionmentioning

confidence: 99%

Forsythoside B ameliorates diabetic cognitive dysfunction by inhibiting hippocampal neuroinflammation and reducing synaptic dysfunction in ovariectomized mice

Nan

Sun

et al. 2022

Front. Aging Neurosci.

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BackgroundDiabetes-associated cognitive impairment (DACI) is a common complication of diabetes, and studies have shown that DACI is more severe in postmenopausal patients with diabetes. Forsythoside B (FTS⋅B) can inhibit inflammation and reduce synaptic dysfunction, which can improve cognitive function. However, it has not been confirmed whether FTS⋅B has a reversing or retarding effect on postmenopausal diabetic encephalopathy.MethodsSeven days after bilateral ovariectomy (OVX) or sham surgery, adult female C57 mice (n = 15/group) received intraperitoneal injection of streptozotocin (60 mg/kg/day/L) and citrate buffer for 5 consecutive days to induce diabetes mellitus (DM). Fourteen days later, ovariectomized diabetic mice were given intraperitoneal injection of FTS⋅B (100, 150 mg/kg/day/L) and subcutaneous injection of 17β-estradiol (1 mg/kg) for 8 weeks [OVX + DM + low-FTS⋅B group (L-F), OVX + DM + high-FTS⋅B group (H-F), and OVX + DM + 17β-estradiol (ER)]. In addition, the following control groups were defined: Sham, OVX, DM, and OVX + DM (O + D). Fasting plasma glucose, body weight and blood insulin levels were determined in each group of mice. Next, their cognitive function was tested through behavioral experiments. Hematoxylin & eosin (H&E) and Nissl staining were used to detect the morphological changes in the hippocampus. The aggregation of amyloid beta (Aβ) and the hyperaggregation of p-tau were assessed by immunohistochemistry. Interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), brain-derived neurotrophic factor (BDNF), post-synaptic density-95 (PSD-95), synaptophysin, and synapsin-1 expression in the hippocampus was detected by real-time polymerase chain reaction (RT-PCR) and western blot analysis.ResultsFTS⋅B can decrease fasting glucose and blood insulin level. Behavioral results showed that cognitive decline was the most severe in the O + D group, and the ER, L-F, and H-F groups revised the cognitive decline. Compared to the O + D group, more normal morphology, which has obvious nucleoli and clear nuclear membrane, was observed by H&E and Nissl staining in the ER, L-F, and H-F groups. FTS⋅B alleviated DACI by reducing the aggregation of Aβ and the hyperaggregation of p-tau in the hippocampus. Moreover, the protein and mRNA expression showed that FTS⋅B not only inhibited inflammation by decreasing IL-1β, IL-6, and TNF-α but also modulated synaptic plasticity by increasing BDNF, PSD-95, synaptophysin, and synapsin-1.ConclusionThese results suggest that FTS⋅B may be a novel therapeutic target for postmenopausal diabetic encephalopathy treatment.

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Section: Discussionmentioning

confidence: 99%

Forsythoside B ameliorates diabetic cognitive dysfunction by inhibiting hippocampal neuroinflammation and reducing synaptic dysfunction in ovariectomized mice

Nan

Sun

et al. 2022

Front. Aging Neurosci.

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“…Upon its translocation to the nucleus, activated CREB endorses the transcription and expression of its target genes BDNF and its cognate receptor TrKB ( Nair and Vaidya, 2006 ; Chou et al, 2020 ). This verity has been mirrored herein, since following the activated cAMP/p-CREB axis, Lira succeeded to oppose the effect of 3-NP and augmented the striatal contents of BDNF and the protein expression of its receptor TrKB.…”

Section: Discussionmentioning

confidence: 99%

Liraglutide Improves Cognitive and Neuronal Function in 3-NP Rat Model of Huntington’s Disease

et al. 2021

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Huntington’s disease (HD) is an autosomal dominant inherited neurodegenerative disease characterized by progressive motor, psychiatric, and cognitive abnormalities. The antidiabetic drug liraglutide possesses a neuroprotective potential against several neurodegenerative disorders; however, its role in Huntington’s disease (HD) and the possible mechanisms/trajectories remain elusive, which is the aim of this work. Liraglutide (200 μg/kg, s.c) was administered to rats intoxicated with 3-nitropropionic acid (3-NP) for 4 weeks post HD model induction. Liraglutide abated the 3-NP-induced neurobehavioral deficits (open field and elevated plus maze tests) and histopathological changes. Liraglutide downregulated the striatal mRNA expression of HSP 27, PBR, and GFAP, while it upregulated that of DARPP32. On the molecular level, liraglutide enhanced striatal miR-130a gene expression and TrKB protein expression and its ligand BDNF, while it reduced the striatal protein content and mRNA expression of the death receptors sortilin and p75NTR, respectively. It enhanced the neuroprotective molecules cAMP, p-PI3K, p-Akt, and p-CREB, besides modulating the p-GSK-3β/p-β-catenin axis. Liraglutide enhanced the antioxidant transcription factor Nrf2, abrogated TBARS, upregulated both Bcl2 and Bcl-XL, and downregulated Bax along with decreasing caspase-3 activity. Therefore, liraglutide exerts a neurotherapeutic effect on 3-NP-treated rats that is, besides the upturn of behavioral and structural findings, it at least partially, increased miR-130a and modulated PI3K/Akt/CREB/BDNF/TrKB, sortilin, and p75NTR, and Akt/GSK-3β/p-β-catenin trajectories besides its capacity to decrease apoptosis and oxidative stress, as well as its neurotrophic activity.

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“…AD is known for the deposition of amyloid β aggregates in the central nervous system and retina, and AMD is known for amyloid β deposits in drusens and the RPE from studies with donor human eyes [ 26 , 31 ]. A cross-sectional study reported that GlcN is associated with beneficial cognitive function [ 32 ] and in in vivo studies, GlcN can increase the level of brain-derived neurotrophic factor, which is involved in memory consolidation and cognitive function [ 33 ]. With these numerous similarities, one can hypothesize that GlcN may be beneficial for patients with AMD as well; however, further research is needed.…”

Section: Discussionmentioning

confidence: 99%

The impact of glucosamine on age-related macular degeneration in patients: A nationwide, population-based cohort study

et al. 2021

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Purpose To analyze the association between glucosamine (GlcN) use and the risk of age-related macular degeneration (AMD) using claims data from the National Health Insurance Research Database (NHIRD). Methods A retrospective, population-based study was conducted with NHIRD data from a 14-year period (2000–2013). Chi-squared and Student’s t-tests were used to evaluate differences between the study and comparison cohorts for categorical and continuous variables, respectively. Risk factors for disease development were examined by the adjusted hazard ratio (aHR) with 95% confidence interval. Kaplan-Meier analysis was performed to compare the cumulative risk of AMD between the two cohorts. Results In total, 1,344 patients with GlcN treatment were enrolled in the study cohort and 5,376 patients without GlcN use were enrolled in the comparison cohort. The incidence rate of AMD was lower with GlcN use (3.65%) than without GlcN use (5.26%) (P = 0.014). GlcN use was associated with a lower risk of developing AMD among patients with hyperlipidemia, coronary artery disease, chronic obstructive pulmonary disease, stroke, other neurological disorders, or degenerative arthritis. Although the incidence of wet type AMD did not significantly differ (P = 0.91), the incidence of dry type AMD was lower in patients with GlcN use (2.9%) than those without GlcN use (4.84%) (P = 0.003). Kaplan-Meier analysis similarly revealed a lower rate of dry type AMD in patients with GlcN use compared to those without GlcN use (log-rank P = 0.004). Conclusions GlcN treatment can decrease the risk of developing dry type AMD. Further prospective controlled studies are needed to determine the effectiveness of GlcN treatment in patients with AMD and the associated mechanism.

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Glucosamine Enhancement of BDNF Expression and Animal Cognitive Function

Cited by 13 publications

References 34 publications

Forsythoside B ameliorates diabetic cognitive dysfunction by inhibiting hippocampal neuroinflammation and reducing synaptic dysfunction in ovariectomized mice

Forsythoside B ameliorates diabetic cognitive dysfunction by inhibiting hippocampal neuroinflammation and reducing synaptic dysfunction in ovariectomized mice

Liraglutide Improves Cognitive and Neuronal Function in 3-NP Rat Model of Huntington’s Disease

The impact of glucosamine on age-related macular degeneration in patients: A nationwide, population-based cohort study

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