Ferulic Acid Improves Synaptic Plasticity and Cognitive Impairments by Alleviating the PP2B/DARPP-32/PP1 Axis-Mediated STEP Increase and Aβ Burden in Alzheimer's Disease

Mahaman, Yacoubou Abdoul Razak; Huang, Fang; Salissou, Maibouge Tanko Mahamane; Yacouba, Mohamed Bassirou Moukeila; Wang, Jian‐Zhi; Liu, Rong; Zhang, Bin; Li, Honglian; Zhu, Feiqi; Wang, Xiaochuan

doi:10.1007/s13311-023-01356-6

Cited by 6 publications

(3 citation statements)

References 156 publications

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“…The fast and efficient clearance of glutamate from the extracellular space following neuronal activity is, therefore, necessary for the spatial and temporal limitation of neuronal activation ( Haj-Yasein et al, 2015 ; Lia et al, 2023 ). The hallmark pathologies of this illness, including amyloid-β buildup, tau hyperphosphorylation, and neuronal death, are brought on by increased intracellular calcium ( Jadiya et al, 2023 ; Mahaman et al, 2023 ). Thus, an increase in the amyloid and Ki-67 protein expression along with the proliferation of astrocyte nuclei and calcium signaling S-100 in the hippocampus regulates the number of processes related to Alzheimer’s disease ( Winkelman and Dai, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

A systematic review of the neuropathology and memory decline induced by monosodium glutamate in the Alzheimer’s disease-like animal model

Ankul,

Chandran,

Anuragh

et al. 2023

Front. Pharmacol.

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This systematic review analyzes monosodium glutamate (MSG) in the Alzheimer’s disease-like condition to enhance translational research. Our review seeks to understand how MSG affects the brain and causes degenerative disorders. Due to significant preclinical data linking glutamate toxicity to Alzheimer’s disease and the lack of a comprehensive review or meta-analysis, we initiated a study on MSG’s potential link. We searched PubMed, ScienceDirect, ProQuest, DOAJ, and Scopus for animal research and English language papers without time constraints. This study used the PRISMA-P framework and PICO technique to collect population, intervention or exposure, comparison, and result data. It was registered in PROSPERO as CRD42022371502. MSG affected mice’s exploratory behaviors and short-term working memory. The brain, hippocampus, and cerebellar tissue demonstrated neuronal injury-related histological and histomorphometric changes. A total of 70% of MSG-treated mice had poor nesting behavior. The treated mice also had more hyperphosphorylated tau protein in their cortical and hippocampus neurons. Glutamate and glutamine levels in the brain increased with MSG, and dose-dependent mixed horizontal locomotor, grooming, and anxiety responses reduced. MSG treatment significantly decreased phospho-CREB protein levels, supporting the idea that neurons were harmed, despite the increased CREB mRNA expression. High MSG doses drastically lower brain tissue and serum serotonin levels. In conclusion, MSG showed AD-like pathology, neuronal atrophy, and short-term memory impairment. Further research with a longer time span and deeper behavioral characterization is needed.Systematic review registration: https://www.crd.york.ac.uk/prospero/, identifier [CRD42022371502].

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Section: Discussionmentioning

confidence: 99%

A systematic review of the neuropathology and memory decline induced by monosodium glutamate in the Alzheimer’s disease-like animal model

Ankul,

Chandran,

Anuragh

et al. 2023

Front. Pharmacol.

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“…Kim et al [ 169 ] highlighted that FA administration (20 or 50 mg/kg bw) for 28 days improved trimethyltin-induced cognitive deficits and increased ChAT activity. Most recently, FA improved behavioral and cognitive function and effectively attenuated Aβ-induced upregulation of intracellular Ca 2+ , inhibited PP1, and activated dopamine and cAMP regulated phosphoprotein 32 kDa (DARPP-32) by increasing synapsin1 and synaptic protein PSD-95 and improving LTP, as well as preventing the loss of GluN2B phosphorylation and decreasing Aβ accumulation in APP/PS1 mice [ 170 ]. Wang et al [ 171 ] reported that FA (20 mg/kg bw) for 30 days reduced Aβ plaque deposition and increased the diameter and density of hippocampal capillaries, thus facilitating the supply of oxygen and nutrients to the brain and the removal of metabolic waste; this led to improved spatial memory in the APP/PS1 AD mouse model.…”

Section: Dietary Small Molecules and Neuroprotection – A Overview Of ...mentioning

confidence: 99%

Development of dietary small molecules as multi-targeting treatment strategies for Alzheimer's disease

Balakrishnan,

Jannat,

Choi

2024

Redox Biology

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“…By 2050, 106.8 million AD patients are expected to exist worldwide, making it a growing public health concern with substantial socioeconomic implications [ 1 ]. Most cases of AD commonly manifest in patients over 65 years old (late-onset AD), with some cases occurring in patients as young as their mid-40s or early 50s (early-onset AD) [ 2 ]. This disorder is described by the production and buildup of amyloid β (Aβ) plaques and tau amyloid fibrils, which lead to synapse loss and neurodegeneration [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Dapagliflozin Ameliorates Cognitive Impairment in Aluminum-Chloride-Induced Alzheimer’s Disease via Modulation of AMPK/mTOR, Oxidative Stress and Glucose Metabolism

et al. 2023

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Alzheimer’s disease (AD) is a progressive neurological illness characterized by memory loss and cognitive deterioration. Dapagliflozin was suggested to attenuate the memory impairment associated with AD; however, its mechanisms were not fully elucidated. This study aims to examine the possible mechanisms of the neuroprotective effects of dapagliflozin against aluminum chloride (AlCl3)-induced AD. Rats were distributed into four groups: group 1 received saline, group 2 received AlCl3 (70 mg/kg) daily for 9 weeks, and groups 3 and 4 were administered AlCl3 (70 mg/kg) daily for 5 weeks. Dapagliflozin (1 mg/kg) and dapagliflozin (5 mg/kg) were then given daily with AlCl3 for another 4 weeks. Two behavioral experiments were performed: the Morris Water Maze (MWM) and the Y-maze spontaneous alternation (Y-maze) task. Histopathological alterations in the brain, as well as changes in acetylcholinesterase (AChE) and amyloid β (Aβ) peptide activities and oxidative stress (OS) markers, were all evaluated. A western blot analysis was used for the detection of phosphorylated 5’ AMP-activated protein kinase (p-AMPK), phosphorylated mammalian target of Rapamycin (p-mTOR) and heme oxygenase-1 (HO-1). Tissue samples were collected for the isolation of glucose transporters (GLUTs) and glycolytic enzymes using PCR analysis, and brain glucose levels were also measured. The current data demonstrate that dapagliflozin represents a possible approach to combat AlCl3-induced AD in rats through inhibiting oxidative stress, enhancing glucose metabolism and activating AMPK signaling.

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Ferulic Acid Improves Synaptic Plasticity and Cognitive Impairments by Alleviating the PP2B/DARPP-32/PP1 Axis-Mediated STEP Increase and Aβ Burden in Alzheimer's Disease

Cited by 6 publications

References 156 publications

A systematic review of the neuropathology and memory decline induced by monosodium glutamate in the Alzheimer’s disease-like animal model

A systematic review of the neuropathology and memory decline induced by monosodium glutamate in the Alzheimer’s disease-like animal model

Development of dietary small molecules as multi-targeting treatment strategies for Alzheimer's disease

Dapagliflozin Ameliorates Cognitive Impairment in Aluminum-Chloride-Induced Alzheimer’s Disease via Modulation of AMPK/mTOR, Oxidative Stress and Glucose Metabolism

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