Relationship of circulatory BDNF with cognitive deficits in people with Parkinson's disease

Khalil, Hanan; Alomari, Mahmoud A.; Khabour, Omar F.; Al-Hieshan, Aya; Bajwa, Jawad A.

doi:10.1016/j.jns.2016.01.032

Cited by 39 publications

(22 citation statements)

References 31 publications

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“…Chronic deprivation of BDNF-TrkB signaling pathway leads to selective late-onset nigrostriatal dopaminergic degeneration ( Baydyuk et al, 2011a ,b). In addition, epidemiological studies showed that low serum levels of BDNF are associated with the motor ( Scalzo et al, 2010 ) and cognitive impairments ( Angelucci et al, 2015 ; Khalil et al, 2016 ; Wang et al, 2016 ) in parkinsonian patients. Thus, novel drugs enhancing the biosynthesis of BDNF are considered to be putative therapeutics to prevent the ongoing neurodegenerative of PD.…”

Section: Discussionmentioning

confidence: 99%

Orexin-A Exerts Neuroprotective Effects via OX1R in Parkinson’s Disease

et al. 2018

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Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by progressive and selective death of dopaminergic neurons. Orexin-A is involved in many biological effects of the body. It has been reported that orexin-A has protective effects in cellular models of PD. However, little is known about the protective effects of orexin-A in animal parkinsonian models and the cellular mechanism has not yet been fully clarified. The aim of this study was to evaluate the effects of orexin-A in MPTP mice model of PD as well as the possible neuroprotective mechanisms of orexin-A on dopaminergic neurons. The results from animal experiments demonstrated that orexin-A attenuated the loss of dopaminergic neurons and the decrease of tyrosine hydroxylase (TH) expression in the substantia nigra, normalized the striatal dopaminergic fibers, and prevented the depletion of dopamine and its metabolites in the striatum. MPTP-treated mice showed cognitive impairments accompanied with significant motor deficiency. Orexin-A improved MPTP-induced impairments in both motor activity and spatial memory. Importantly, orexin-A increased the protein level of brain-derived neurotrophic factor (BDNF) in dopaminergic neurons of the substantia nigra. Furthermore, the protective effects of orexin-A on MPTP parkinsonian mice could be blocked by orexinergic receptor 1 (OX1R) antagonist, SB334867. In another set of experiments with SH-SY5Y dopaminergic cells, orexin-A significantly induced the expression of BDNF in a dose and time-dependent manner. The upregulation of BDNF is mainly concerned with PI3K and PKC signaling pathways via OX1R. The present study demonstrated that orexin-A exerted neuroprotective effects on MPTP parkinsonian mice, which may imply orexin-A as a potential therapeutic target for PD.

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Section: Discussionmentioning

confidence: 99%

Orexin-A Exerts Neuroprotective Effects via OX1R in Parkinson’s Disease

et al. 2018

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“…Because BDNF is an important mediator for neuronal survival and synaptic plasticity to maintain brain functions, possible contribution of BDNF/TrkB dysfunction in the cognitive deficits in PD patients was hypothesized. Positive correlations between serum BDNF concentration and severity of the symptoms [ 134 , 135 ] and cognitive deficits [ 136 , 137 ] in the patients with PD have been reported. Reduced levels of BDNF mRNA [ 12 ] and protein [ 13 ] in the substantia nigra of the postmortem PD patients were also demonstrated.…”

Section: Parkinson’s Disease and Bdnfmentioning

confidence: 99%

Actions of Brain-Derived Neurotrophin Factor in the Neurogenesis and Neuronal Function, and Its Involvement in the Pathophysiology of Brain Diseases

Numakawa

Odaka

Adachi

2018

IJMS

246

138

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It is well known that brain-derived neurotrophic factor, BDNF, has an important role in a variety of neuronal aspects, such as differentiation, maturation, and synaptic function in the central nervous system (CNS). BDNF stimulates mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK), phosphoinositide-3kinase (PI3K), and phospholipase C (PLC)-gamma pathways via activation of tropomyosin receptor kinase B (TrkB), a high affinity receptor for BDNF. Evidence has shown significant contributions of these signaling pathways in neurogenesis and synaptic plasticity in in vivo and in vitro experiments. Importantly, it has been demonstrated that dysfunction of the BDNF/TrkB system is involved in the onset of brain diseases, including neurodegenerative and psychiatric disorders. In this review, we discuss actions of BDNF and related signaling molecules on CNS neurons, and their contributions to the pathophysiology of brain diseases.

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“…It should be mentioned that due to genetic pleiotropy, both COMT and BDNF have been found to be associated with several other aspects of cognition beyond WM, including reaction time (Das et al, 2014), cognitive flexibility (Kang et al, 2013), aging-related cognitive degradation (Ghisletta et al, 2014; Voelcker-Rehage et al, 2015), executive function (Leckie et al, 2014; Sapkota et al, 2015), and neurocognitive deficits in people with schizophrenia (Ahmed et al, 2015) or Parkinson's disease (Khalil et al, 2016). Nevertheless, WM has been the main focus of the previous literature in this field.…”

Section: Introductionmentioning

confidence: 99%

Interaction Effects of BDNF and COMT Genes on Resting-State Brain Activity and Working Memory

Chen

Xia

et al. 2016

Front. Hum. Neurosci.

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Catechol-O-methyltransferase (COMT) and brain-derived neurotrophic factor (BDNF) genes have been found to interactively influence working memory (WM) as well as brain activation during WM tasks. However, whether the two genes have interactive effects on resting-state activities of the brain and whether these spontaneous activations correlate with WM are still unknown. This study included behavioral data from WM tasks and genetic data (COMT rs4680 and BDNF Val66Met) from 417 healthy Chinese adults and resting-state fMRI data from 298 of them. Significant interactive effects of BDNF and COMT were found for WM performance as well as for resting-state regional homogeneity (ReHo) in WM-related brain areas, including the left medial frontal gyrus (lMeFG), left superior frontal gyrus (lSFG), right superior and medial frontal gyrus (rSMFG), right medial orbitofrontal gyrus (rMOFG), right middle frontal gyrus (rMFG), precuneus, bilateral superior temporal gyrus, left superior occipital gyrus, right middle occipital gyrus, and right inferior parietal lobule. Simple effects analyses showed that compared to other genotypes, subjects with COMT-VV/BDNF-VV had higher WM and lower ReHo in all five frontal brain areas. The results supported the hypothesis that COMT and BDNF polymorphisms influence WM performance and spontaneous brain activity (i.e., ReHo).

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Relationship of circulatory BDNF with cognitive deficits in people with Parkinson's disease

Cited by 39 publications

References 31 publications

Orexin-A Exerts Neuroprotective Effects via OX1R in Parkinson’s Disease

Orexin-A Exerts Neuroprotective Effects via OX1R in Parkinson’s Disease

Actions of Brain-Derived Neurotrophin Factor in the Neurogenesis and Neuronal Function, and Its Involvement in the Pathophysiology of Brain Diseases

Interaction Effects of BDNF and COMT Genes on Resting-State Brain Activity and Working Memory

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