Brain-Derived Neurotrophic Factor Expression in Individuals With Schizophrenia and Healthy Aging: Testing the Accelerated Aging Hypothesis of Schizophrenia

Islam, Farhana; Mulsant, Benoit H.; Voineskos, Aristotle N.; Rajji, Tarek K.

doi:10.1007/s11920-017-0794-6

Cited by 46 publications

(33 citation statements)

References 88 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, elevated hippocampal levels of BNDF have been reported (66). These changes are highly pertinent to schizophrenia, as NDMA hypofunction and decreased BDNF levels are thought to be involved in its pathogenesis, and its associated cognitive impairment (67).…”

Section: Prebiotics In Schizophreniamentioning

confidence: 99%

The Gut Microbiome and Schizophrenia: The Current State of the Field and Clinical Applications

et al. 2020

View full text Add to dashboard Cite

Section: Prebiotics In Schizophreniamentioning

confidence: 99%

The Gut Microbiome and Schizophrenia: The Current State of the Field and Clinical Applications

et al. 2020

View full text Add to dashboard Cite

“…Morphological changes such as reduction in dendritic order and TDL have also been observed. These alterations coexist with the decline in the expression of neurotrophic factors, such as BDNF and an increase in reactive astrogliosis (Islam, Mulsant, Voineskos, & Rajji, ; Jyothi et al, ). All this is an indication of the evolution of a neurodegenerative process in limbic regions culminating with neuronal death and the deterioration of spatial and/or recognition memory (Diaz et al, ; Johnson et al, ; Vidal et al, ).…”

Section: Discussionmentioning

confidence: 99%

The neuropeptide‐12 improves recognition memory and neuronal plasticity of the limbic system in old rats

Hernández-Hernández

Hernandez

Vázquez-Roque

et al. 2018

Synapse

View full text Add to dashboard Cite

Aging is a stage of life where cognitive and motor functions are impaired. This is because oxidative and inflammatory processes exacerbate neurodegeneration, which affects dendritic morphology and neuronal communication of limbic regions with memory loss. Recently, the use of trophic substances has been proposed to prevent neuronal deterioration. The neuropeptide-12 (N-PEP-12) has been evaluated in elderly patients with dementia, showing improvements in cognitive tasks due to acts as a neurotrophic factor. In the present work, we evaluated the effect of N-PEP-12 on motor activity and recognition memory, as well as its effects on dendritic morphology and the immunoreactivity of GFAP, Synaptophysin (SYP), and BDNF in neurons of the prefrontal cortex (PFC), dorsal hippocampus (DH) and nucleus accumbens (NAcc) of aged rats. The results show that N-PEP-12 improved the recognition memory, but the motor activity was not modified compared to the control animals. N-PEP-12 increases the density of dendritic spines and the total dendritic length in neurons of the PFC (layers 3 and 5) and in DH (CA1 and CA3). Interestingly NAcc neurons showed a reduction in the number of dendritic spines. In the N-PEP-12 animals, when evaluating the immunoreactivity for SYP and BDNF, there was an increase in the three brain regions, while the mark for GFAP decreased significantly. Our results suggest that N-PEP-12 promotes neuronal plasticity in the limbic system of aged animals, which contributes to improving recognition memory. In this sense, N-PEP-12 can be considered as a pharmacological alternative to prevent or delay brain aging and control senile dementias.

show abstract

“…BDNF has a role in regulating the secretion of neurotransmitters with a key effect on serotonergic, dopaminergic, glutamatergic, and plasticity mechanisms such as long-term potential and mechanisms in learning and memory [9]. Many studies have shown a close link between BDNF and some diseases like schizophrenia, Alzheimer's disease, mood disorders, and Parkinson's disease [10][11][12][13][14]. Some studies have shown that BDNF probably has a necessary role in neuroimmune regulation of mood disorders.…”

Section: Introductionmentioning

confidence: 99%

Cigarette Smoking Reduces BDNF in Heavy Smokers

Miladpour¹,

Mohammadian²,

Kavousipour³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Cigarette smoke is a powerful environmental modifier of DNA methylation. BDNF is a neurotrophin family of growth factors and is important in growth, progression, regeneration, survival, maintenance, and function of neurons. In this study, we aimed to evaluate the epigenetic changes, serum level, and gene expression of BDNF, in cigarette smokers. Methods: To assess the BDNF DNA methylation, peripheral blood samples were obtained from 237 cigarette smokers and 90 healthy nonsmokers as controls. DNA methylation was evaluated with MS-PCR. Gene expression and serum level were carried out with qRT-PCR and ELISA assay respectively. Results: The results from MS-PCR showed that DNA methylation of BDNF gene is more significant in heavy smokers than healthy nonsmokers as control (p-value <0.05). Serum level of BDNF and gene expression is significantly lower in heavy smokers than in healthy nonsmokers (p-value <0.05). Conclusion: In conclusion, heavy smoking can modify BDNF gene epigenetics. The serum levels of BDNF and the gene expression decreases in heavy smokers compared to healthy nonsmokers.

show abstract

Brain-Derived Neurotrophic Factor Expression in Individuals With Schizophrenia and Healthy Aging: Testing the Accelerated Aging Hypothesis of Schizophrenia

Cited by 46 publications

References 88 publications

The Gut Microbiome and Schizophrenia: The Current State of the Field and Clinical Applications

The Gut Microbiome and Schizophrenia: The Current State of the Field and Clinical Applications

The neuropeptide‐12 improves recognition memory and neuronal plasticity of the limbic system in old rats

Cigarette Smoking Reduces BDNF in Heavy Smokers

Contact Info

Product

Resources

About