Serum levels of insulin-like growth factor-1 and brain-derived neurotrophic factor as potential recovery biomarkers in stroke

King, Michael; Kelly, Liam; Wallack, Elizabeth M.; Hasan, S M Mahmudul; Kirkland, Megan C.; Curtis, Marie E; Chatterjee, Tanaya; McCarthy, Jason; Ploughman, Michelle

doi:10.1080/01616412.2018.1564451

Cited by 24 publications

(38 citation statements)

References 78 publications

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“…Terminal measurements of brain BDNF protein demonstrated that six-week neflamapimod treatment resulted in dose-dependent increases of this neurotrophic factor in both the injured and uninjured hemisphere. BDNF is a key regulator of plasticity both in the healthy and injured brain which has been recognized as a key regulator of rehabilitation-and activityinduced functional and motor recovery, respectively, after stroke [74][75][76]. BDNF is reported to have a critical role in promoting recovery after stroke as a crucial signaling molecule that mediates adaptive brain plasticity [22,[77][78][79][80].…”

Section: Plos Onementioning

confidence: 99%

Continuous administration of a p38α inhibitor during the subacute phase after transient ischemia-induced stroke in the rat promotes dose-dependent functional recovery accompanied by increase in brain BDNF protein level

Krakovsky

Germann²,

Levy

2020

PLoS ONE

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There is unmet need for effective stroke therapies. Numerous neuroprotection attempts for acute cerebral ischemia have failed and as a result there is growing interest in developing therapies to promote functional recovery through increasing synaptic plasticity. For this research study, we hypothesized that in addition to its previously reported role in mediating cell death during the acute phase, the alpha isoform of p38 mitogen-activated protein kinase, p38α, may also contribute to interleukin-1β-mediated impairment of functional recovery during the subacute phase after acute ischemic stroke. Accordingly, an oral, brain-penetrant, small molecule p38α inhibitor, neflamapimod, was evaluated as a subacute phase stroke treatment to promote functional recovery. Neflamapimod administration to rats after transient middle cerebral artery occlusion at two dose levels was initiated outside of the previously characterized therapeutic window for neuroprotection of less than 24 hours for p38α inhibitors. Six-week administration of neflamapimod, starting at 48 hours after reperfusion, significantly improved behavioral outcomes assessed by the modified neurological severity score at Week 4 and at Week 6 post stroke in a dose-dependent manner. Neflamapimod demonstrated beneficial effects on additional measures of sensory and motor function. It also resulted in a dose-related increase in brain-derived neurotrophic factor (BDNF) protein levels, a previously reported potential marker of synaptic plasticity that was measured in brain homogenates at sacrifice. Taken together with literature evidence on the role of p38α-dependent suppression by interleukin-1β of BDNF-mediated synaptic plasticity and BDNF production, our findings support a mechanistic model in which inhibition of p38α promotes functional recovery after ischemic stroke by blocking the deleterious effects of interleukin-1β on synaptic plasticity. The dose-related in vivo efficacy of neflamapimod offers the possibility of having a therapy for stroke that could be initiated outside the short time window for neuroprotection and for improving recovery after a completed stroke.

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Section: Plos Onementioning

confidence: 99%

Continuous administration of a p38α inhibitor during the subacute phase after transient ischemia-induced stroke in the rat promotes dose-dependent functional recovery accompanied by increase in brain BDNF protein level

Krakovsky

Germann²,

Levy

2020

PLoS ONE

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“…The study's critical finding is that serum BDNF levels were independently associated with mortality in patients who did not feature detectable brain dysfunction [11]. Another study has found that increased BDNF levels indicate positive patient rehabilitation and are associated with physical and cognitive recovery [12].…”

Section: Discussionmentioning

confidence: 99%

Assessment of BNP and BDNF results in elective endovascular cerebral aneurysm treatment

Sukun

Çekiç

2021

Ir J Med Sci

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Background B-type natriuretic peptide (BNP) levels increase with an increase in intracranial pressure. A decrease in BNP levels has been found to be associated with patient positive prognosis. Brain-derived neurotrophic factor (BDNF) levels decrease in patients with acute stroke. Aims To compare the BNP and BDNF values in serum before and after elective endovascular cerebral aneurysm treatment (ECAT). Methods A total of 50 patients who underwent elective ECAT were included in the study. Exclusion criteria were determined to be history of heart failure or heart attack (n = 8), renal failure (n = 5), subarachnoid hemorrhage (n = 4), or previous aneurysm clip procedure (n = 3). Intravenous blood samples were obtained from 30 patients who underwent elective ECAT before and after treatment. After centrifugation, the BNP and BDNF values in serum were obtained with the ELISA method and compared. Results This study included 19 female and 11 male patients, aged between 24 and 75 years. The average age of the patients was 51.27 ± 13.31 years. The median BDNF values did not change significantly after ECAT (before the endovascular procedure: 3.1 ± 1.3 pg/dl; after the endovascular procedure: 2.8 ± 0.9 pg/dl, p = 0.16). Median BNP levels decreased significantly after ECAT (before the endovascular procedure: 617.50 ± 483.11 pg/ml; after the endovascular procedure: 395.00 ± 352.15 pg/ml, p < 0.001). Conclusions After elective endovascular cerebral aneurysm treatment, the BNP values in serum decreased significantly, and the BDNF values in serum did not change significantly. Keywords BDNF • BNP • Cerebral aneurysm • Endovascular treatment Abbreviations BNPB-type natriuretic peptide BDNF Brain-derived neurotrophic factor ECAT Endovascular cerebral aneurysm treatment

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“…This process, presumably the major mechanism of neuroplasticity, is responsible for learning and memory as well as development and response of the brain to injuries [ 20 ]. Studies involving animals with stroke show increased brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I) and nerve growth factor (NGF) after physical exercise [ 17 , 21 , 22 ]; these factors all contribute to reduction of neurons loss and growth of synaptic connections in multiple brain regions [ 11 ]. Physical exercise regulates numerous supporting systems of neuroplasticity, including neurogenesis, synaptogenesis, cerebral metabolism and angiogenesis [ 23 ].…”

Section: Physical Exercise Enhances Neuroplasticitymentioning

confidence: 99%

Neuroplastic Effect of Exercise Through Astrocytes Activation and Cellular Crosstalk

Li¹,

Xu²,

Yun³

et al. 2021

Aging and disease

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Physical exercise is an effective therapy for neurorehabilitation. Exercise has been shown to induce remodeling and proliferation of astrocyte. Astrocytes potentially affect the recruitment and function of neurons; they could intensify responses of neurons and bring more neurons for the process of neuroplasticity. Interactions between astrocytes, microglia and neurons modulate neuroplasticity and, subsequently, neural circuit function. These cellular interactions promote the number and function of synapses, neurogenesis, and cerebrovascular remodeling. However, the roles and crosstalk of astrocytes with neurons and microglia and any subsequent neuroplastic effects have not been studied extensively in exercise-induced settings. This article discusses the impact of physical exercise on astrocyte proliferation and highlights the interplay between astrocytes, microglia and neurons. The crosstalk between these cells may enhance neuroplasticity, leading to the neuroplastic effects of exercise.

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Serum levels of insulin-like growth factor-1 and brain-derived neurotrophic factor as potential recovery biomarkers in stroke

Cited by 24 publications

References 78 publications

Continuous administration of a p38α inhibitor during the subacute phase after transient ischemia-induced stroke in the rat promotes dose-dependent functional recovery accompanied by increase in brain BDNF protein level

Continuous administration of a p38α inhibitor during the subacute phase after transient ischemia-induced stroke in the rat promotes dose-dependent functional recovery accompanied by increase in brain BDNF protein level

Assessment of BNP and BDNF results in elective endovascular cerebral aneurysm treatment

Neuroplastic Effect of Exercise Through Astrocytes Activation and Cellular Crosstalk

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