Cognitive impairment and BDNF serum levels

Siuda, Joanna; Patalong‐Ogiewa, Maja; Żmuda, Weronika; Targosz-Gajniak, Magdalena; Niewiadomska, Ewa; Matuszek, Iwona; Jędrzejowska–Szypułka, Halina; Rudzińska‐Bar, Monika

doi:10.1016/j.pjnns.2016.10.001

Cited by 99 publications

(69 citation statements)

References 55 publications

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“…Brain‐derived neurotrophic factor is a neuropeptide deeply involved in neuronal survival as well as in learning and memory (Almeida et al , ). In addition, BDNF gene expression is significantly decreased in AD patients (Peng et al , ) and possibly related to the cognitive impairments (Siuda et al , ). Our finding of increased BDNF gene expression is consistent with a possible protective effect related to Harpagophytum extract treatment.…”

Section: Resultsmentioning

confidence: 99%

Protective Effects Induced by Microwave-Assisted Aqueous Harpagophytum Extract on Rat Cortex Synaptosomes Challenged with Amyloid β-Peptide

et al. 2017

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Harpagophytum procumbens is a plant species that displays anti-inflammatory properties in multiple tissues. The iridoid glycosides arpagoside, harpagide, and procumbide appear to be the most therapeutically important constituents. In addition, harpagoside treatment exerted neuroprotective effects both in vitro and in vivo. Considering these findings, the aim of the present work is to explore the possible protective role of the previously described microwave-assisted aqueous extract of H. procumbens on rat hypothalamic (Hypo-E22) cells, and in rat cortex challenged with amyloid β-peptide (1-40). In this context, we assayed the protective effects induced by H. procumbens by measuring the levels of malondialdehyde, 3-hydroxykynurenine (3-HK), brain-derived neurotrophic factor, and tumor necrosis factor-α, 3-HK. Finally, we evaluated the effects of H. procumbens treatment on cortex levels of dopamine, norepinephrine, and serotonin. H. procumbens extract was well tolerated by Hypo-E22 cells and upregulated brain-derived neurotrophic factor gene expression but down-regulated tumor necrosis factor-α gene expression. In addition, the extract reduced amyloid β-peptide stimulation of malondialdehyde and 3-HK and blunted the decrease of dopamine, norepinephrine, and serotonin, in the cortex. In this context, our work supports further studies for the evaluation and confirmation of Harpagophytum in the management of the clinical symptoms related to Alzheimer's disease. Copyright © 2017 John Wiley & Sons, Ltd.

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Section: Resultsmentioning

confidence: 99%

Protective Effects Induced by Microwave-Assisted Aqueous Harpagophytum Extract on Rat Cortex Synaptosomes Challenged with Amyloid β-Peptide

et al. 2017

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“…Advanced age and low education has been associated with decreased serum BDNF levels, with the lowest levels in patients with AD, which also corresponded to the severity of cognitive impairment 41 . Others have observed that at early stages of AD, BDNF significantly increased in comparison to control groups although levels then declined in later stages of the disease whereas another study found no change in BDNF 42 .…”

Section: Neuronal Injury/death Biomarkers In Ad and Deliriummentioning

confidence: 97%

Delirium and Alzheimer disease: A proposed model for shared pathophysiology

Fong

Vasunilashorn

Libermann

et al. 2019

Int J Geriat Psychiatry

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“…A decrease in BDNF levels in the blood and brain was observed in patients with depression or suffering from PD and AD [59][60][61][62]. Decreased BDNF concentration in serum and brain is accompanied by an increase in degeneration of dopaminergic neurons in PD, which leads to movement disorders, cognitive deficit, and mental disorders [63][64][65][66] and also correlates with memory impairment in AD [67,68]. There are data indicating that a decrease in BDNF levels in PD may contribute to overexpression of alpha-synuclein (ASN) and inhibition of dopamine (DA) synthesis [69][70][71].…”

Section: Role Of Bdnf In Neurodegeneration and Neuroregenerationmentioning

confidence: 99%

BDNF as a Promising Therapeutic Agent in Parkinson’s Disease

Pałasz

Wysocka

Gąsiorowska

et al. 2020

IJMS

296

197

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Brain-derived neurotrophic factor (BDNF) promotes neuroprotection and neuroregeneration. In animal models of Parkinson's disease (PD), BDNF enhances the survival of dopaminergic neurons, improves dopaminergic neurotransmission and motor performance. Pharmacological therapies of PD are symptom-targeting, and their effectiveness decreases with the progression of the disease; therefore, new therapeutical approaches are needed. Since, in both PD patients and animal PD models, decreased level of BDNF was found in the nigrostriatal pathway, it has been hypothesized that BDNF may serve as a therapeutic agent. Direct delivery of exogenous BDNF into the patient's brain did not relieve the symptoms of disease, nor did attempts to enhance BDNF expression with gene therapy. Physical training was neuroprotective in animal models of PD. This effect is mediated, at least partly, by BDNF. Animal studies revealed that physical activity increases BDNF and tropomyosin receptor kinase B (TrkB) expression, leading to inhibition of neurodegeneration through induction of transcription factors and expression of genes related to neuronal proliferation, survival, and inflammatory response. This review focuses on the evidence that increasing BDNF level due to gene modulation or physical exercise has a neuroprotective effect and could be considered as adjunctive therapy in PD.

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Cognitive impairment and BDNF serum levels

Abstract: Advanced age and low educational level are associated with decreased BDNF serum levels. Decreased BDNF serum levels correspond to the severity of cognitive impairment. There is no correlation between BDNF serum levels and depressive symptoms.

Cited by 99 publications

References 55 publications

Protective Effects Induced by Microwave-Assisted Aqueous Harpagophytum Extract on Rat Cortex Synaptosomes Challenged with Amyloid β-Peptide

Protective Effects Induced by Microwave-Assisted Aqueous Harpagophytum Extract on Rat Cortex Synaptosomes Challenged with Amyloid β-Peptide

Delirium and Alzheimer disease: A proposed model for shared pathophysiology

BDNF as a Promising Therapeutic Agent in Parkinson’s Disease

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