Roles of brain-derived neurotrophic factor/tropomyosin-related kinase B (BDNF/TrkB) signalling in Alzheimer’s disease

Zhang, Fang; Kang, Zhilong; Li, Wen; Xiao, Zhi‐Cheng; Zhou, Xin‐Fu

doi:10.1016/j.jocn.2011.12.022

Cited by 90 publications

(53 citation statements)

References 61 publications

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“…Exploring beyond BDNF, a growth factor whose links to AD has been asserted [46,47], genes whose expressions are statistically tied to BDNF expression in transcriptional regulatory networks are prime candidates for further scrutiny (see Jimenez et al [48]). Of the nodes linked to BDNF in the ARACNe-derived whole mouse brain network ( Supplementary Fig.…”

Section: Discussionmentioning

confidence: 99%

A Regulatory Role for the Insulin- and BDNF-Linked RORA in the Hippocampus: Implications for Alzheimer's Disease

Acquaah‐Mensah

Agu

Khan

et al. 2015

JAD

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Abstract. Alzheimer's disease (AD) is the leading cause of dementia. The etiology of AD remains, in large part, unresolved. In this study, gene expression (microarray) data from postmortem brains in normal aged as well as AD-affected brains in conjunction with transcriptional regulatory networks were explored for etiological insights. The focus was on the hippocampus, a brain region key to memory and learning. The transcriptional regulatory networks were inferred using a trees-based (random forests or extra-trees) as well as a mutual information-based algorithm applied to compendia of adult mouse whole brain and hippocampus microarray data. Network nodes representing human orthologs of the mouse networks were used in the subsequent analysis. Among the potential transcriptional regulators tied to insulin or brain-derived neurotrophic factor (INS1, INS2, BDNF), whose peptide products have been linked to AD, is the Retinoic Acid Receptor-Related Orphan Receptor (RORA). RORA is a nuclear receptor transcription factor whose expression is distinctly upregulated in the AD hippocampus. A notable cross-section of genes differentially expressed in the AD hippocampus was found to be linked to RORA in the networks. Furthermore, several genes associated with RORA in the networks, such as APP, DNM1L, and TIA1 have been implicated in AD. Computationallyderived clusters and modules within the networks indicated strong ties between RORA and genes involved in the AD etiology. In addition, a functional mapping scheme using activity and interaction data affirmed the same network links to RORA. Thus, RORA emerges as a gene with a probable central role in the AD pathology/etiology.

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Section: Discussionmentioning

confidence: 99%

A Regulatory Role for the Insulin- and BDNF-Linked RORA in the Hippocampus: Implications for Alzheimer's Disease

Acquaah‐Mensah

Agu

Khan

et al. 2015

JAD

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“…NGF, the first identified neurotrophin, was remarkably able to reduce the neurodegeneration of cholinergic neurons in fimbria transection [95,96]. Additionally, it partially reduced the cholinergic atrophy in aged rodents [97].…”

Section: Neurochemicals Behaviours and Psychiatric Perspectives Of Nmentioning

confidence: 93%

“…Additionally, it partially reduced the cholinergic atrophy in aged rodents [97]. Altered levels of BDNF and its receptor, Tropomyosin receptor kinase B (TrkB) in the entorhinal cortex (EC) and the frontal cortex (FC) are related to impairments in memory and cognition associated with AD [95], Down Syndrome [96], and aging [97]. PD is associated with reduced BDNF levels at both the transcript and protein levels in the dopaminergic neurons of the substantia nigra [98].…”

Section: Neurochemicals Behaviours and Psychiatric Perspectives Of Nmentioning

confidence: 99%

Neurochemicals, Behaviours and Psychiatric Perspectives of Neurological Diseases

Choudhury¹,

Sahu²,

Ramanujam³

et al. 2018

Neuropsychiatry

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Structural changes in different regions of the brain have become clinically relevant and regarded as the signature phenomenon for neurological diseases. Morphological changes in brain are also associated with neuronal and neurochemical alterations. Studies have showed that minute changes in neurochemical levels may have marked impact on the psychobehaviour of the subject. Several neurological disease profiles have been reported with such specific psychobehavioural expression. However, application of behavioural abnormalities as possible disease progress markers has not been considered and emphasised much. Reports suggested that-the subjects, who have already entered into the terminal stage of the disease, used to show cardinal behavioural signs for a specific disease profile. However, psychological expressions are comparatively early expressive. As most of the neurodegenerative disorders are unidirectional and progressive by nature, therapeutic intervention at the right time is essential for attaining the desired outcome. Moreover, early diagnosis can aid in managing the disease progression also. Psychobehavioural analysis could meet the expected outcome of disease diagnosis if implemented properly and timely. In the present review, we have amalgamated the reported behavioural anomalies with the supportive background from neurochemical basis. Further, we have concluded that behaviour centric studies could be a potential diagnostic tool for the early diagnosis of major neurological diseases such as Alzheimer disease, Parkinson's disease, Amyotrophic lateral sclerosis (ALS), Bipolar disorder, Schizophrenia, Impulse control disorder (ICD) and Obsessive-compulsive disorder (OCD).

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“…Because of their crucial roles in neuron, it is easy to imagine that impairment of these receptors would have a major impact on neuronal activities. Down-regulation or defects of these receptors are suspected to be involved in depression [23,24] , and Alzheimer's disease [25] .…”

Section: Neurotrophin Receptorsmentioning

confidence: 99%

Effect of the Sigma-1 receptor on neurite outgrowth

Kimura¹,

Fujita²,

Yamashita³

2014

Receptor Clin Invest

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Neurite outgrowth is one of the essential processes underlying development and plasticity of the nervous system. Enhancing neurite outgrowth, along with neural protection, is one of the most prominent therapeutic strategies against neuronal degeneration or damage. The sigma-1 receptor (Sig-1R) is a brain-enriched a receptor chaperone expressed in the ER membrane. As Sig-1R is involved in the mode of action of several neurotherapeutic drugs, it is important to elucidate the molecular mechanism of Sig-1R. This would increase our understanding of the pathology of neuronal diseases as well as aid in establishing new approaches for their treatment. In this review, we focus on the findings that Sig-1R contributes to neural protection and neurite outgrowth even in pathological conditions, such as in high glutamate concentration. Although a large part of molecular mechanisms of Sig-1R remains unknown, the interaction of Sig-1R and neurotrophin receptors has been recently reported. Activation of Sig-1R leads to an increase in the secretion of neurotrophin. Meanwhile, Sig-1R enhances neurotrophin receptor-mediated neurite outgrowth upon activation. We discuss the neurite outgrowth effect of Sig-1R, especially in relation to neurotrophin-mediated neurite outgrowth.

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Roles of brain-derived neurotrophic factor/tropomyosin-related kinase B (BDNF/TrkB) signalling in Alzheimer’s disease

Cited by 90 publications

References 61 publications

A Regulatory Role for the Insulin- and BDNF-Linked RORA in the Hippocampus: Implications for Alzheimer's Disease

A Regulatory Role for the Insulin- and BDNF-Linked RORA in the Hippocampus: Implications for Alzheimer's Disease

Neurochemicals, Behaviours and Psychiatric Perspectives of Neurological Diseases

Effect of the Sigma-1 receptor on neurite outgrowth

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