Amelioration of Parkinson's disease by pharmacological inhibition and knockdown of redox sensitive TRPC5 channels: Focus on mitochondrial health

Vaidya, Bhupesh; Gupta, Pankaj; Laha, Joydev K.; Roy, Ipsita; Sharma, Shyam Sunder

doi:10.1016/j.lfs.2023.121871

Cited by 9 publications

(4 citation statements)

References 66 publications

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“…copper [154]; iron [155]; zinc [156] Copper [157]; iron [158] Mitochondria and metabolic functions MCL1 [159] ROCK [160], δ-opioid receptor [161] Mutated/misfolded proteins Amyloid-β [162]; β-secretase [163]; γ-secretase [164]; GSK3-β [165]; RAGE [166]; Tau [167] DJ1 [168]; LRRK2 [169]; Pink1 [170]; αsynuclein [171]; CK1δ [172]; CK1δ+GSK3b [173] Neuroinflammation NRLP3 inflammasome [174] Adenosine receptors [175]; cannabinoid receptor 2 [176]; monoacylglycerol lipase [177]; NRLP3 Inflammasome [178]; PPAR [179]; TRPC5 [180] Neuroprotection Apoptosis [181]; ferroptosis [182]; sigma 1 and 2 receptors [183] Apoptosis [184]; autophagy/neuroinflammation [185]; CDNF peptidomimetic [186]; ferroptosis [187]; nurr1 [188]; sigma 1 and 2 receptors [189] Oxidative stress Antioxidants [190]; NRF2 signaling pathway [191] Aldose reductase [192]; NRF2 signaling pathway [193] Synaptic activity AChE [110]; α7nAChR [194]; butyrylcholinesterase…”

Section: Metal Dyshomeostasismentioning

confidence: 99%

Drug Development for Alzheimer’s and Parkinson’s Disease: Where Do We Go Now?

Sequeira,

Benfeito,

Fernandes

et al. 2024

Pharmaceutics

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Neurodegenerative diseases (NDs) are a set of progressive, chronic, and incurable diseases characterized by the gradual loss of neurons, culminating in the decline of cognitive and/or motor functions. Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common NDs and represent an enormous burden both in terms of human suffering and economic cost. The available therapies for AD and PD only provide symptomatic and palliative relief for a limited period and are unable to modify the diseases’ progression. Over the last decades, research efforts have been focused on developing new pharmacological treatments for these NDs. However, to date, no breakthrough treatment has been discovered. Hence, the development of disease-modifying drugs able to halt or reverse the progression of NDs remains an unmet clinical need. This review summarizes the major hallmarks of AD and PD and the drugs available for pharmacological treatment. It also sheds light on potential directions that can be pursued to develop new, disease-modifying drugs to treat AD and PD, describing as representative examples some advances in the development of drug candidates targeting oxidative stress and adenosine A2A receptors.

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Section: Metal Dyshomeostasismentioning

confidence: 99%

Drug Development for Alzheimer’s and Parkinson’s Disease: Where Do We Go Now?

Sequeira,

Benfeito,

Fernandes

et al. 2024

Pharmaceutics

View full text Add to dashboard Cite

show abstract

“…monoacylglycerol lipase [175]; NRLP3 Inflammasome [176]; PPAR [177]; TRPC5 [178] Neuroprotection Apoptosis [179]; ferroptosis [180]; sigma 1 and 2 receptors [181] Apoptosis [182];…”

Section: Mitochondria and Metabolic Functionsmentioning

confidence: 99%

Drug Development for Alzheimer’s and Parkinson’s Disease: Where Do We Go Now?

Sequeira,

Benfeito,

Fernandes

et al. 2024

Preprint

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Neurodegenerative diseases (NDs) are a set of progressive, chronic, and incurable diseases characterized by the gradual loss of neurons, culminating in the decline of cognitive and/or motor functions. Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common NDs and represent an enormous burden both in terms of human suffering and economic cost. The available therapies for AD and PD only provide symptomatic and palliative relief for a limited period and are unable to modify the diseases’ progression. Over the last decades, research efforts have been focused on developing new pharmacological treatments for these NDs. However, to date, no breakthrough treatment has been discovered. Hence, the development of disease-modifying drugs able to halt or reverse the progression of NDs remains an unmet clinical need. This review summarizes the major hallmarks of AD and PD and the drugs available for pharmacological treatment. It also sheds light on potential directions that can be pursued to develop of new, disease-modifying drugs to treat AD and PD, thereby decreasing the social and economic burdens linked to these NDs.

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“…The rats not entering the dark chamber during the acquisition trial were not considered for further experiments. After 24 h, a retention trial was performed, and latency to step into the dark compartment was recorded without the foot shock (Vaidya et al, 2023;Yadav et al, 2023).…”

Section: Passive Avoidance Testmentioning

confidence: 99%

Aerobic exercise and metformin co-administration attenuate the cognitive impairment in an experimental model of type 2 diabetes mellitus: Focus on neuroinflammation and adult hippocampal neurogenesis

Padhy,

Aggarwal,

Ravichandiran

et al. 2024

Preprint

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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that increases the prevalence of cognitive impairment in the elderly. Aerobic exercise has been reported as an excellent non-pharmacological therapeutic strategy to prevent Alzheimer’s disease and dementia. The present study assessed the role of treadmill exercise and metformin (70 mg/kg) co-administration for fourteen weeks in cognitive impairment and its associated molecular mechanism in T2DM rats. Neurobehavioural assessments were performed to evaluate spatial recognition and fear-conditioned memory. ELISA was performed to evaluate the inflammatory cytokines in the hippocampus of diabetic rats. Furthermore, immunohistochemistry and western blotting confirmed the effect of exercise and metformin on astrogliosis and adult hippocampal neurogenesis. T2DM rats showed a significant alteration in neurobehavioural patterns compared to the control group, which were improved in the exercise and metformin co-administered animals. The level of neuroinflammation was significantly elevated in the hippocampal tissue of T2DM rats compared to the control and lowered after exercise and metformin treatment. Molecular expression of mature neurons, astrogliosis, microgliosis, and neurogenesis markers were significantly altered in T2DM rat brains and ameliorated upon exercise and metformin treatment. Moreover, upregulation of the canonical Wnt/β-catenin pathway in the hippocampus was observed in exercise and metformin co-administered rats, which was impaired in the T2DM hippocampus. In summary, long-term aerobic exercise with metformin treatment ameliorated neuroinflammation and promoted adult hippocampal neurogenesis via upregulating the canonical Wnt/β-catenin pathway in T2DM rats.

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Amelioration of Parkinson's disease by pharmacological inhibition and knockdown of redox sensitive TRPC5 channels: Focus on mitochondrial health

Cited by 9 publications

References 66 publications

Drug Development for Alzheimer’s and Parkinson’s Disease: Where Do We Go Now?

Drug Development for Alzheimer’s and Parkinson’s Disease: Where Do We Go Now?

Drug Development for Alzheimer’s and Parkinson’s Disease: Where Do We Go Now?

Aerobic exercise and metformin co-administration attenuate the cognitive impairment in an experimental model of type 2 diabetes mellitus: Focus on neuroinflammation and adult hippocampal neurogenesis

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