BDNF serum and CSF concentrations in Alzheimer’s disease, normal pressure hydrocephalus and healthy controls

Laske, Christoph; Stransky, Elke; Leyhe, Thomas; Eschweiler, Gerhard W.; Maetzler, Walter; Wittorf, Andreas; Soekadar, Surjo R.; Richartz, Elke; Koehler, Niklas; Bartels, M.; Buchkremer, Gerhard; Schott, Klaus

doi:10.1016/j.jpsychires.2006.01.014

Cited by 242 publications

(163 citation statements)

References 45 publications

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“…For example, levels of brain BDNF have been shown to correlate with human learning, memory and cognitive function (205)(206)(207) . Future efforts should focus on whether the ability of flavonoids to induce improvements in cognition is mediated by their ability to induce BDNF and/or other neurotrophin production in either the brain or the periphery (Fig.…”

Section: Present and Future Perspectivesmentioning

confidence: 99%

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

Spencer

2010

Proc. Nutr. Soc.

143

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The consumption of flavonoid-rich foods and beverages has been suggested to limit the neurodegeneration associated with a variety of neurological disorders and to prevent or reverse normal or abnormal deteriorations in cognitive performance. Flavonoids mediate these effects via a number of routes, including a potential to protect neurons against injury induced by neurotoxins, an ability to suppress neuroinflammation and a potential to promote memory, learning and cognitive function. Originally, it was thought that such actions were mediated by the antioxidant capacity of flavonoids. However, their limited absorption and their low bioavailability in the brain suggest that this explanation is unlikely. Instead, this multiplicity of effects appears to be underpinned by three separate processes: first, through their interactions with important neuronal and glial signalling cascades in the brain, most notably the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways that regulate prosurvival transcription factors and gene expression; second, through an ability to improve peripheral and cerebral blood flow and to trigger angiogenesis and neurogenesis in the hippocampus; third, by their capacity to directly react with and scavenge neurotoxic species and pro-inflammatory agents produced in the brain as a result of both normal and abnormal brain ageing. The present review explores the potential inhibitory or stimulatory actions of flavonoids within these three systems and describes how such interactions are likely to underlie neurological effects.

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Section: Present and Future Perspectivesmentioning

confidence: 99%

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

Spencer

2010

Proc. Nutr. Soc.

143

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“…Multiple studies have revealed a drop in BDNF levels in AD patients (156)(157)(158)(159), while other reports indicate an increase in BNDF expression compared to control (160), which could be a compensatory repair mechanism during early stages of AD. Overall, it has been hypothesized that activating BDNF intracellular signaling could be a promising strategy in AD treatment (151).…”

Section: Neurotrophic and Hematopoietic Growth Factors Brain-derived mentioning

confidence: 99%

Alzheimer’s Disease: Dawn of a New Era?

et al. 2017

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Alzheimer’s disease (AD) is an irreversible neurodegenerative disease characterized by a progressive decline in cognition and memory, leading to significant impairment in daily activities and ultimately death. It is the most common cause of dementia, the prevalence of which increases with age; however, age is not the only predisposing factor. The pathology of this cognitive impairing disease is still not completely understood, which has limited the development of valid therapeutic options. Recent years have witnessed a wide range of novel approaches to combat this disease, so that they greatly increased our understanding of the disease and of the unique drug development issues associated with this disease. In this paper, we provide a brief overview of the history, the clinical presentation and diagnosis, and we undertake a comprehensive review of the various approaches that have been brought to clinical trials in recent years, including immunotherapeutic approaches, tau-targeted strategies, neurotransmitter-based therapies, neurotropic and hematopoietic growth factors, and antioxidant therapies, trying to highlight the lessons learned from these approaches. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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“…It must determine whether the correlation between SD and neurodegenerative processes is indeed a causal one, and if it is, which mechanisms are involved. It has been shown that memory impairments are related to the excessive production of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α), which is observed in distinct pathological conditions, namely, neurodegenerative diseases (21). Decreased serum brain-derived neurotrophic factor (BDNF) is also evident in Alzheimer's disease.…”

Section: Introductionmentioning

confidence: 99%

“…Decreased serum brain-derived neurotrophic factor (BDNF) is also evident in Alzheimer's disease. This bioelement plays its role in preventing neurodegeneration, thus, tends to decline in exposure to chronic oxidative stress conditions (21,22). With regard to SD, we hypothesized that the decreased BDNF may reflect either enhanced neuronal demand for BDNF or its declined production due to the inflammatory processes following SD.…”

Section: Introductionmentioning

confidence: 99%

Aversive Memory, Anxiety-Related Behaviors, and Serum Neurochemical Levels in a Rat Model of Labored Sleep Loss

et al. 2014

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Background: Sleep deprivation (SD) is emerging as a hot topic due to its health concerns. There are compelling reasons for a tremendous interest in neuroscience of sleep in recent years. Objectives: We aimed to evaluate how total sleep deprivation (TSD) and chronic partial sleep restriction (CPSR) might affect memory, anxiety-related behaviors, and the serum level of neurochemical markers such as brain-derived neurotrophic factor (BDNF) and corticosterone in a rat model. Materials and Methods:The disk-over-water (DOW) apparatus was employed to induce TSD and CPSR in male Wistar rats. The six study arms were as follows: cage control, 48 hours; cage control, seven days; DOW control, 48 hours; DOW control, seven days, TSD, and CPSR. Elevated plus-maze (EPM) was used to measure parameters (percentage of OAT, percentage of OAE, and locomotor activity) corresponding to anxiety and aversive memory. To measure serum BDNF and corticosterone levels using the ELISA method, blood samples were drawn from all rats on the fourth day at 5 P.M. Results: Our results demonstrated that TSD (P < 0.001) and CPSR (P < 0.001) induce memory impairment while exert anxiolytic-like effects in comparison with controls. Data showed that CPSR causes more memory impairment and anxiolytic-like effect in comparison to TSD (P < 0.001).These interventions however, did not alter the locomotor activity. Serum corticosterone level raised dramatically in CPSR rats in comparison to TSD and controls. Although the difference in serum BDNF level between TSD and CPSR arms was insignificant, it was markedly decreased in comparison to corresponding controls (P < 0.001). Conclusions: Our findings suggest the more pronounced effect of CPSR rather than TSD in impairing aversive memory and reducing anxiety. Decreased BDNF and peaked corticosterone level in TSD and CPSR suggest the probable inflammatory processes involved in possible insults to the brain caused by SD.

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BDNF serum and CSF concentrations in Alzheimer’s disease, normal pressure hydrocephalus and healthy controls

Cited by 242 publications

References 45 publications

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

Alzheimer’s Disease: Dawn of a New Era?

Aversive Memory, Anxiety-Related Behaviors, and Serum Neurochemical Levels in a Rat Model of Labored Sleep Loss

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