Insights on benzodiazepines' potential in Alzheimer's disease

Al-Kuraishy, Hayder M; Al-Gareeb, Ali I; Alsayegh, Abdulrahman A.; Abusudah, Wafaa Fouzi; Almohmadi, Najlaa Hamed; Eldahshan, Omayma A.; Ahmed, Eman; Batiha, Gaber El‐Saber

doi:10.1016/j.lfs.2023.121532

Cited by 19 publications

(7 citation statements)

References 115 publications

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“… 21 The primary cause of Lewy bodies is the deposition of α‐Syn, which is also present in other neurological conditions known as synucleinopathies. 22 Notably, substantia nigra motor dopaminergic neurons are lost by 70% before Parkinson's disease symptoms appear.…”

Section: Pathogenesis and Clinical Feature Of Pdmentioning

confidence: 99%

“… 46 , 47 , 48 AD neuropathology is characterized by extracellular accumulation of mutant amyloid beta (Aβ) peptide and intracellular accumulation of hyper‐phosphorylated tau protein which form neurofibrillary tangles (NFTs). 22 , 49 , 50 , 51 Of note, synaptic abnormalities are involved in AD neuropathology and linked with disease severity and progression of Aβ and NFTs. Both Aβ and NFTs alter the synapses and neuronal circuit resulting in cognitive dysfunction and impairment of the synthesis and the release of BDNF from brain neurons.…”

Section: Bdnf and Neurodegenerative Diseasesmentioning

confidence: 99%

“…The neuropathology of Parkinson's disease (PD) arises from the gradual deterioration of dopaminergic neurons located in the substantia nigra, as well as the build‐up of Lewy bodies within the survival motor neurons 21 . The primary cause of Lewy bodies is the deposition of α‐Syn, which is also present in other neurological conditions known as synucleinopathies 22 . Notably, substantia nigra motor dopaminergic neurons are lost by 70% before Parkinson's disease symptoms appear.…”

Section: Pathogenesis and Clinical Feature Of Pdmentioning

confidence: 99%

“…Alzheimer's disease is the most prevalent neurodegenerative disease characterized by cognitive impairment and memory dysfunction 46–48 . AD neuropathology is characterized by extracellular accumulation of mutant amyloid beta (Aβ) peptide and intracellular accumulation of hyper‐phosphorylated tau protein which form neurofibrillary tangles (NFTs) 22,49–51 . Of note, synaptic abnormalities are involved in AD neuropathology and linked with disease severity and progression of Aβ and NFTs.…”

Section: Bdnf and Neurodegenerative Diseasesmentioning

confidence: 99%

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BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy

Ali,

Al‐Kuraishy,

Al‐Gareeb

et al. 2024

J Cellular Molecular Medi

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Parkinson's disease (PD) is a neurodegenerative disorder of the brain and is manifested by motor and non‐motor symptoms because of degenerative changes in dopaminergic neurons of the substantia nigra. PD neuropathology is associated with mitochondrial dysfunction, oxidative damage and apoptosis. Thus, the modulation of mitochondrial dysfunction, oxidative damage and apoptosis by growth factors could be a novel boulevard in the management of PD. Brain‐derived neurotrophic factor (BDNF) and its receptor tropomyosin receptor kinase type B (TrkB) are chiefly involved in PD neuropathology. BDNF promotes the survival of dopaminergic neurons in the substantia nigra and enhances the functional activity of striatal neurons. Deficiency of the TrkB receptor triggers degeneration of dopaminergic neurons and accumulation of α‐Syn in the substantia nigra. As well, BDNF/TrkB signalling is reduced in the early phase of PD neuropathology. Targeting of BDNF/TrkB signalling by specific activators may attenuate PD neuropathology. Thus, this review aimed to discuss the potential role of BDNF/TrkB activators against PD. In conclusion, BDNF/TrkB signalling is decreased in PD and linked with disease severity and long‐term complications. Activation of BDNF/TrkB by specific activators may attenuate PD neuropathology.

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Section: Pathogenesis and Clinical Feature Of Pdmentioning

confidence: 99%

Section: Bdnf and Neurodegenerative Diseasesmentioning

confidence: 99%

Section: Pathogenesis and Clinical Feature Of Pdmentioning

confidence: 99%

Section: Bdnf and Neurodegenerative Diseasesmentioning

confidence: 99%

See 2 more Smart Citations

BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy

Ali,

Al‐Kuraishy,

Al‐Gareeb

et al. 2024

J Cellular Molecular Medi

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“…On the other hand, there is no effective treatment method for the disease, and commonly used clinical drugs(statins, benzodiazepines, metformin, etc.) are prohibitive for patients due to their severe adverse reactions such as hypotension and involuntary movements [ [14] , [15] , [16] , [17] ]. Therefore, exploring new therapeutic drugs has become an urgent problem to be solved.…”

Section: Introductionmentioning

confidence: 99%

Integrated network pharmacology and phosphoproteomic analyses of Baichanting in Parkinson's disease model mice

Gao,

Fu,

et al. 2024

Heliyon

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Hypoglycemia and Alzheimer Disease Risk: The Possible Role of Dasiglucagon

Ali,

Al-Kuraishy,

Al-Gareeb

et al. 2024

Cell Mol Neurobiol

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Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by memory impairment and cognitive dysfunctions. It has been shown that hypoglycemia can adversely affect AD neuropathology. It is well-known that chronic hyperglycemia in type 2 diabetes (T2D) is regarded as a potential risk factor for the development and progression of AD. However, the effect of recurrent hypoglycemia on the pathogenesis of AD was not deeply discussed, and how recurrent hypoglycemia affects AD at cellular and molecular levels was not intensely interpreted by the previous studies. The underlying mechanisms for hypoglycaemia-induced AD are diverse such as endothelial dysfunction, thrombosis, and neuronal injury that causing tau protein hyperphosphorylation and the accumulation of amyloid beta (Aβ) in the brain neurons. Of note, the glucagon hormone, which controls blood glucose, can also regulate the cognitive functions. Glucagon increases blood glucose by antagonizing the metabolic effect of insulin. Therefore, glucagon, through attenuation of hypoglycemia, may prevent AD neuropathology. Glucagon/GLP-1 has been shown to promote synaptogenesis, hippocampal synaptic plasticity, and learning and memory, while attenuating amyloid and tau pathologies. Therefore, activation of glucagon receptors in the brain may reduce AD neuropathology. A recent glucagon receptor agonist dasiglucagon which used in the management of hypoglycemia may be effective in preventing hypoglycemia and AD neuropathology. This review aims to discuss the potential role of dasiglucagon in treating hypoglycemia in AD, and how this drug reduce AD neuropathology.

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Insights on benzodiazepines' potential in Alzheimer's disease

Cited by 19 publications

References 115 publications

BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy

BDNF/TrkB activators in Parkinson's disease: A new therapeutic strategy

Integrated network pharmacology and phosphoproteomic analyses of Baichanting in Parkinson's disease model mice

Hypoglycemia and Alzheimer Disease Risk: The Possible Role of Dasiglucagon

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