Evaluation of the DNA methylation of brain-derived neurotrophic factor (bdnf) gene promoter I as a biomarker in psychiatric disorders

Abstract Adolescent suicide research has mostly focused on demographic risk factors. Such studies focus on who is at risk, but do not explain why certain adolescents are at risk for suicide. Studies of the neurobiology of adolescent suicide could clarify why some youths are more suicidal than others and help to find biological markers of suicidal behavior in teenagers. Over the past decade the role of brain-derived neurotrophic factor (BDNF) in the pathophysiology of suicidal behavior has attracted significant attention of scientists. BDNF is involved in the pathophysiology of many psychiatric disorders associated with suicidal behavior including depression, post-traumatic stress disorder, schizophrenia, and obsessive-compulsive disorder. BDNF dysregulation could be associated with increased suicidality independently of psychiatric diagnoses. BDNF plays an important role in the regulation and growth of neurons during childhood and adolescence. Prominent among the brain regions undergoing developmental change during adolescence are stressor-sensitive areas. The serotonin dysfunction found in adolescent and adult suicidal behavior could be related to the low level of BDNF, which impedes the normal development of serotonin neurons during brain development. BDNF dysfunction could play a more significant role in the pathophysiology of psychiatric disorders and suicidal behavior in adolescents than in adults. Treatment-induced enhancement in the BDNF function could reduce suicidal behavior secondary to the improvement in psychiatric pathology or independently of improvement in psychiatric disorders. It is interesting to hypothesize that BDNF could be a biological marker of suicidal behavior in adolescents or in certain adolescent populations.

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A novel knockout mouse model of the noncoding antisense Brain-Derived Neurotrophic Factor (Bdnf) gene displays increased endogenous Bdnf protein and improved memory function following exercise

Heliyon ◽

10.1016/j.heliyon.2021.e07570 ◽

2021 ◽

pp. e07570

Author(s):

Farzaneh Modarresi ◽

Roya Pedram-Fatemi ◽

Seyedeh Fatemeh Razavipour ◽

Natalie Ricciardi ◽

Madina Makhmutova ◽

...

Keyword(s):

Mouse Model ◽

Neurotrophic Factor ◽

Knockout Mouse ◽

Memory Function ◽

Brain Derived Neurotrophic Factor ◽

Bdnf Gene ◽

Knockout Mouse Model

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Brain-Derived Neurotrophic Factor Systemic Response in the Periodontium, Trigeminal Nucleus Caudalis, and Hippocampus Induced by Occlusal Trauma

Journal of Biomedical Nanotechnology ◽

10.1166/jbn.2021.3112 ◽

2021 ◽

Vol 17 (7) ◽

pp. 1371-1379

Author(s):

Di Liu ◽

Ying Li ◽

Jiechen Liu ◽

Zhiyuan Shen ◽

Fengying Wang ◽

...

Keyword(s):

Neurotrophic Factor ◽

Brain Derived Neurotrophic Factor ◽

Systemic Response ◽

Periodontal Tissue ◽

Trigeminal Nucleus ◽

Bdnf Gene ◽

Dental Tissue ◽

Injury And Repair ◽

Activity Dependent ◽

The Brain

Occlusal trauma (OT), by causing periodontal tissue damage, can activate and enhance the activity of the peripheral and central nervous system (CNS) neuropeptides. The brain-derived neurotrophic factor (BDNF) gene is activity-dependent and exhibits marked alterations, characterized by protection against injury and repair. Our results show the possible molecular mechanism through which noxious environmental stimuli induce alterations in BDNF activity in the local periodontal tissue, the primary sensory neurons-Vc, and the hippocampus, suggesting systemic impairment. BDNF serves a more positive and enduring trauma protection and repair function in Vc compared to that in local dental tissue.

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