Cerebrospinal fluid BDNF pro-peptide levels in major depressive disorder and schizophrenia

Mizui, Toshiyuki; Hattori, Kotaro; Ishiwata, Sayuri; Hidese, Shinsuke; Yoshida, Sumiko; Kunugi, Hiroshi; Kojima, Masami

doi:10.1016/j.jpsychires.2019.03.024

Cited by 35 publications

(26 citation statements)

References 53 publications

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“…As a result, we could reach multivariate kurtosis value to 4.143, although it did not mean normality (< 1), but moderate non-normality (< 10) by excluding proBDNF from the SEM analysis. Although the strength of our study is its measurements of both proBDNF and BDNF in each subject, the newly identified BDNF pro-peptide-proBDNF is cleaved to BDNF and this BDNF pro-peptide 41 -was not measured, leaving the possibility that BDNF pro-peptide could interfere with the statistical effects of proBDNF on memory function.…”

Section: Discussionmentioning

confidence: 99%

Lower brain-derived neurotrophic factor levels are associated with age-related memory impairment in community-dwelling older adults: the Sefuri study

Mizoguchi

Yao

Imamura

et al. 2020

Sci Rep

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The beneficial effects of brain-derived neurotrophic factor (BDNF)—a member of the neurotrophin family—on cognitive function or dementia are well established in both rodents and human beings. In contrast, little is known about the association of proBDNF—a precursor protein with opposing neuronal effects of BDNF—with cognitive function in non-demented older adults. We analyzed brain magnetic resonance imaging findings of 256 community-dwelling older adults (mean age of 68.4 years). Serum BDNF and proBDNF levels were measured by quantitative enzyme-linked immunosorbent assay. Logistic regression analysis revealed that older age, less physical activity, hippocampal atrophy, and lower BDNF levels were independently associated with memory impairment determined by the Rivermead Behavioral Memory Test. Path analysis based on structural equation modeling indicated that age, sport activity, hippocampal atrophy and BDNF but not proBDNF were individually associated with Rivermead Behavioral Memory Test scores. These findings suggest that impaired BDNF function, in addition to physical inactivity and hippocampal atrophy, is associated with age-related memory impairment. Therefore, BDNF may be a potential target for dementia prevention.

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Section: Discussionmentioning

confidence: 99%

Lower brain-derived neurotrophic factor levels are associated with age-related memory impairment in community-dwelling older adults: the Sefuri study

Mizoguchi

Yao

Imamura

et al. 2020

Sci Rep

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“…Thus, cleavage of proBDNF could have occurred in the present study, which suggests that proBDNF affects microglial cellular functions. The newly identified BDNF pro-peptide, proBDNF that is cleaved to mature BDNF and this BDNF pro-peptide (Mizui et al, 2019), was not examined, raising the possibility that BDNF pro-peptide could have influenced our findings.…”

Section: Discussionmentioning

confidence: 99%

ProBDNF induces sustained elevation of intracellular Ca²⁺ possibly mediated by TRPM7 channels in rodent microglial cells

Mizoguchi

Ohgidani

Haraguchi

et al. 2021

Glia

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Microglia are intrinsic immune cells that release factors including pro‐ and anti‐inflammatory cytokines, nitric oxide (NO) and neurotrophins following activation in the brain. Elevation of intracellular Ca2+ concentration ([Ca2+]i) is important for microglial functions, such as the release of cytokines or NO from activated microglia. Brain‐derived neurotrophic factor (BDNF) is a neurotrophin well known for its roles in the activation of microglia. Interestingly, proBDNF, the precursor form of mature BDNF, and mature BDNF elicit opposing neuronal responses in the brain. Mature BDNF induces sustained intracellular Ca2+ elevation through the upregulation of the surface expression of TRPC3 channels in rodent microglial cells. In addition, TRPC3 channels are important for the BDNF‐induced suppression of NO production in activated microglia. In this study, we observed that proBDNF and mature BDNF have opposite effects on the relative expression of surface p75 neurotrophin receptor (p75NTR) in rodent microglial cells. ProBDNF induces a sustained elevation of [Ca2+]i through binding to the p75NTR, which is possibly mediated by Rac 1 activation and TRPM7 channels in rodent microglial cells. Flow cytometry showed that proBDNF increased the relative surface expression of TRPM7. Although proBDNF did not affect either mRNA expression of pro‐ and anti‐inflammatory cytokines or the phagocytic activity, proBDNF potentiates the generation of NO induced by IFN‐γ and TRPM7 channels could be involved in the proBDNF‐induced potentiation of IFN‐γ‐mediated production of NO. We show direct evidence that rodent microglial cells are able to respond to proBDNF, which might be important for the regulation of inflammatory responses in the brain.

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“…In particular, specific antibody and sensitive immunoassay methods were recently useful. The release from cells into culture media can conventionally be measured for BDNF (Anastasia et al 2013, Katoh-Semba et al 1999, Kolbeck et al 1999, Matsumoto et al 2008, Rauskolb, Zagrebelsky, Dreznjak, Deogracias, Matsumoto, Wiese, Erne, Sendtner, Schaeren-Wiemers, Korte and Barde, 2010, its pro-peptide (BDNF pro-peptide) (Dieni, Matsumoto, Dekkers, Rauskolb, Ionescu, Deogracias, Gundelfinger, Kojima, Nestel, Frotscher and Barde, 2012, Mizui et al 2019, Mizui et al 2015, and proBDNF (Yang, Siao, Nagappan, Marinic, Jing, McGrath, Chen, Mark, Tessarollo, Lee, Lu and Hempstead, 2009). To detect the endogenous BDNF pro-peptide in Western blotting, membrane fixation with glutaraldehyde was technically effective (Dieni, Matsumoto, Dekkers, Rauskolb, Ionescu, Deogracias, Gundelfinger, Kojima, Nestel, Frotscher and Barde, 2012, Matsumoto et al 2008, Mizui et al 2019, Mizui et al 2015.…”

Section: Biochemical Detection and Imaging Of Bdnf Releasementioning

confidence: 99%

Journey of brain-derived neurotrophic factor: from intracellular trafficking to secretion

et al. 2020

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Brain-derived neurotrophic factor (BDNF) is known to control a wide variety of brain functions, ranging from memory formation to food intake. However, since the BDNF levels are extremely low in the nervous system, the dynamics in neurons from intracellular trafficking to secretion is absolutely complicated; the understanding is not fully promoted. We here review the findings of those critical mechanisms from intracellular trafficking to the secretion of BDNF. Furthermore, to solve this issue, technological advances for the detection, measurement, and imaging of this growth factor are essential. We believe that this review helps the study of these complex but critical mechanisms of BDNF.

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Cerebrospinal fluid BDNF pro-peptide levels in major depressive disorder and schizophrenia

Cited by 35 publications

References 53 publications

Lower brain-derived neurotrophic factor levels are associated with age-related memory impairment in community-dwelling older adults: the Sefuri study

Lower brain-derived neurotrophic factor levels are associated with age-related memory impairment in community-dwelling older adults: the Sefuri study

ProBDNF induces sustained elevation of intracellular Ca²⁺ possibly mediated by TRPM7 channels in rodent microglial cells

Journey of brain-derived neurotrophic factor: from intracellular trafficking to secretion

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Cerebrospinal fluid BDNF pro-peptide levels in major depressive disorder and schizophrenia

Cited by 35 publications

References 53 publications

Lower brain-derived neurotrophic factor levels are associated with age-related memory impairment in community-dwelling older adults: the Sefuri study

Lower brain-derived neurotrophic factor levels are associated with age-related memory impairment in community-dwelling older adults: the Sefuri study

ProBDNF induces sustained elevation of intracellular Ca2+ possibly mediated by TRPM7 channels in rodent microglial cells

Journey of brain-derived neurotrophic factor: from intracellular trafficking to secretion

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ProBDNF induces sustained elevation of intracellular Ca²⁺ possibly mediated by TRPM7 channels in rodent microglial cells