BDNF Val66Met polymorphism and cognitive impairment in Parkinson’s disease—a meta-analysis

Yin, Yanying; Su, Xuening; Pan, Lishou; Li, Chen

doi:10.1007/s10072-019-03907-2

Cited by 15 publications

(7 citation statements)

References 24 publications

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“…The BDNF Val66Met polymorphism has been associated with cerebral cortex plasticity [ 117 , 118 ], with gray matter structures [ 119 , 120 ], or white matter integrities and structural networks [ 121 , 122 ]. More specifically, BDNF Val66Met polymorphism is associated with cognitive processes [ 112 , 123 , 124 , 125 , 126 , 127 ], and cognitive impairment in neurodegenerative disease, such as Parkinson’s disease (PD) [ 128 , 129 ] and AD [ 130 , 131 ], and even more with several brain disorders, including MDD and bipolar disorder [ 132 , 133 , 134 , 135 , 136 , 137 ], epilepsy [ 138 , 139 , 140 ], schizophrenia [ 125 , 141 , 142 , 143 , 144 ], aging and dementia [ 145 ] and stroke [ 117 , 146 , 147 ]. Met66, but not Val66, BDNF pro-domain can induce the growth cone retraction in young hippocampal neurons [ 148 ].…”

Section: The Human Bdnf Gene: Transcripts and Variantsmentioning

confidence: 99%

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Colucci-D’Amato

Speranza

Volpicelli

2020

IJMS

481

249

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Brain-derived neurotrophic factor (BDNF) is one of the most distributed and extensively studied neurotrophins in the mammalian brain. BDNF signals through the tropomycin receptor kinase B (TrkB) and the low affinity p75 neurotrophin receptor (p75NTR). BDNF plays an important role in proper growth, development, and plasticity of glutamatergic and GABAergic synapses and through modulation of neuronal differentiation, it influences serotonergic and dopaminergic neurotransmission. BDNF acts as paracrine and autocrine factor, on both pre-synaptic and post-synaptic target sites. It is crucial in the transformation of synaptic activity into long-term synaptic memories. BDNF is considered an instructive mediator of functional and structural plasticity in the central nervous system (CNS), influencing dendritic spines and, at least in the hippocampus, the adult neurogenesis. Changes in the rate of adult neurogenesis and in spine density can influence several forms of learning and memory and can contribute to depression-like behaviors. The possible roles of BDNF in neuronal plasticity highlighted in this review focus on the effect of antidepressant therapies on BDNF-mediated plasticity. Moreover, we will review data that illustrate the role of BDNF as a potent protective factor that is able to confer protection against neurodegeneration, in particular in Alzheimer’s disease. Finally, we will give evidence of how the involvement of BDNF in the pathogenesis of brain glioblastoma has emerged, thus opening new avenues for the treatment of this deadly cancer.

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Section: The Human Bdnf Gene: Transcripts and Variantsmentioning

confidence: 99%

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Colucci-D’Amato

Speranza

Volpicelli

2020

IJMS

481

249

View full text Add to dashboard Cite

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“…BDNF Met66 polymorphism also affects the activity-dependent release of the BDNF protein, thus reducing the amount of BDNF that is delivered to synapses [99]. Previous research linked the BDNF Met66 polymorphism to altered brain functionalities and psychological capacities among cognitive [100][101][102][103][104] and emotional domains [105,106].…”

Section: Bdnf In Health and Diseasementioning

confidence: 99%

“…For instance, BDNF Met66 polymorphism was recently associated with a higher risk of cognitive impairment in PD [101,103], bipolar disorder [105], and depression [106]. In contrast, a controversial involvement of the BDNF Met66 variant has been described in AD.…”

Section: Bdnf In Health and Diseasementioning

confidence: 99%

Putting Cells in Motion: Advantages of Endogenous Boosting of BDNF Production

Brattico

Bonetti

Ferretti

et al. 2021

Cells

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Motor exercise, such as sport or musical activities, helps with a plethora of diseases by modulating brain functions in neocortical and subcortical regions, resulting in behavioural changes related to mood regulation, well-being, memory, and even cognitive preservation in aging and neurodegenerative diseases. Although evidence is accumulating on the systemic neural mechanisms mediating these brain effects, the specific mechanisms by which exercise acts upon the cellular level are still under investigation. This is particularly the case for music training, a much less studied instance of motor exercise than sport. With regards to sport, consistent neurobiological research has focused on the brain-derived neurotrophic factor (BDNF), an essential player in the central nervous system. BDNF stimulates the growth and differentiation of neurons and synapses. It thrives in the hippocampus, the cortex, and the basal forebrain, which are the areas vital for memory, learning, and higher cognitive functions. Animal models and neurocognitive experiments on human athletes converge in demonstrating that physical exercise reliably boosts BDNF levels. In this review, we highlight comparable early findings obtained with animal models and elderly humans exposed to musical stimulation, showing how perceptual exposure to music might affect BDNF release, similar to what has been observed for sport. We subsequently propose a novel hypothesis that relates the neuroplastic changes in the human brains after musical training to genetically- and exercise-driven BDNF levels.

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“…Аналогичные данные были получены и в другом исследовании [24]. Генотип AA (Met/Met) полиморфизма rs6265 не только влияет на осложнения длительной терапии БП, но и увеличивает шансы развития когнитивных нарушений в 3,8 раза [25]. В настоящее время связи данного полиморфизма с ранним или поздним началом БП не обнаружено [26].…”

Section: ген моноаминооксидазы типа в (мао-в)unclassified

Pharmacogenetics of drug-induced dyskinesias in Parkinson's disease

Tappakhov

Попова

Govorova

et al. 2020

RJTAO

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В изучении патогенеза болезни Паркинсона (БП) достигнуты большие успехи, определена роль недофаминергических систем мозга в клинической картине заболевания, внедрены нейрохирургические вмешательства на глубинных структурах головного мозга, однако препараты леводопы продолжают оставаться «золотым» стандартом лечения данной патологии [1, 2]. Неизбежным осложне-нием леводопа-терапии является развитие лекарственных дискинезий (ЛД), моторных и немоторных флюктуаций, что значительно ограничивает терапевтические возможности данной группы препаратов, ухудшает качество жизни пациентов и требует корректировки лечения [3-5]. Так, ЛД встречаются примерно у 30% пациентов через 5 лет и у 59-100% через 10 лет после начала леводопа-терапии [6].

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BDNF Val66Met polymorphism and cognitive impairment in Parkinson’s disease—a meta-analysis

Cited by 15 publications

References 24 publications

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer

Putting Cells in Motion: Advantages of Endogenous Boosting of BDNF Production

Pharmacogenetics of drug-induced dyskinesias in Parkinson's disease

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