Towards a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking
Brain-derived neurotrophic factor (BDNF) represents promotesa key molecule for the survival and differentiation of specific populations of neurons in the central nervous system. BDNF also regulates plasticity-related processes underlying memory and learning. A common single nucleotide polymorphism (...
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2013-10-01
|
| Series: | Frontiers in Neuroscience |
| Subjects: | |
| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnins.2013.00188/full |
| _version_ | 1818351345540792320 |
|---|---|
| author | Gabriele eBaj Davide eCarlino Lucia eGardossi Enrico eTongiorgi |
| author_facet | Gabriele eBaj Davide eCarlino Lucia eGardossi Enrico eTongiorgi |
| author_sort | Gabriele eBaj |
| collection | DOAJ |
| description | Brain-derived neurotrophic factor (BDNF) represents promotesa key molecule for the survival and differentiation of specific populations of neurons in the central nervous system. BDNF also regulates plasticity-related processes underlying memory and learning. A common single nucleotide polymorphism (SNP) rs6265 has been identified on the coding sequence of human BDNF located at 11p13. The SNP rs6265 is a single base mutation with an adenine instead of a guanine at position 196 (G196A), resulting in the amino acid substitution Val66Met. This polymorphism only exists in humans and has been associated with a plethora of effects ranging from molecular, cellular and brain structural modifications in association with deficits in social and cognitive functions. To date, the literature on Val66Met polymorphism describes a complex and often conflicting pattern of effects. In this review, we attempt to provide a unifying model of the Val66Met effects. We discuss the clinical evidence of the association between Val66Met and memory deficits, as well as the molecular mechanisms involved including the reduced transport of BDNF mRNA to the dendrites as well as the reduced processing and secretion of BDNF protein through the regulated secretory pathway. |
| first_indexed | 2024-12-13T18:36:16Z |
| format | Article |
| id | doaj.art-233fa6d4b94f429f88de6bf1e57927b9 |
| institution | Directory Open Access Journal |
| issn | 1662-453X |
| language | English |
| last_indexed | 2024-12-13T18:36:16Z |
| publishDate | 2013-10-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neuroscience |
| spelling | doaj.art-233fa6d4b94f429f88de6bf1e57927b92022-12-21T23:35:21ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2013-10-01710.3389/fnins.2013.0018863706Towards a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA traffickingGabriele eBaj0Davide eCarlino1Lucia eGardossi2Enrico eTongiorgi3University of TriesteUniversity of TriesteUniversity of TriesteUniversity of TriesteBrain-derived neurotrophic factor (BDNF) represents promotesa key molecule for the survival and differentiation of specific populations of neurons in the central nervous system. BDNF also regulates plasticity-related processes underlying memory and learning. A common single nucleotide polymorphism (SNP) rs6265 has been identified on the coding sequence of human BDNF located at 11p13. The SNP rs6265 is a single base mutation with an adenine instead of a guanine at position 196 (G196A), resulting in the amino acid substitution Val66Met. This polymorphism only exists in humans and has been associated with a plethora of effects ranging from molecular, cellular and brain structural modifications in association with deficits in social and cognitive functions. To date, the literature on Val66Met polymorphism describes a complex and often conflicting pattern of effects. In this review, we attempt to provide a unifying model of the Val66Met effects. We discuss the clinical evidence of the association between Val66Met and memory deficits, as well as the molecular mechanisms involved including the reduced transport of BDNF mRNA to the dendrites as well as the reduced processing and secretion of BDNF protein through the regulated secretory pathway.http://journal.frontiersin.org/Journal/10.3389/fnins.2013.00188/fullBDNFPost-traumatic stress disorderneurotrophinsmemory deficitshippocampus atrophydendritic mRNA trafficking |
| spellingShingle | Gabriele eBaj Davide eCarlino Lucia eGardossi Enrico eTongiorgi Towards a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking Frontiers in Neuroscience BDNF Post-traumatic stress disorder neurotrophins memory deficits hippocampus atrophy dendritic mRNA trafficking |
| title | Towards a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking |
| title_full | Towards a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking |
| title_fullStr | Towards a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking |
| title_full_unstemmed | Towards a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking |
| title_short | Towards a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking |
| title_sort | towards a unified biological hypothesis for the bdnf val66met associated memory deficits in humans a model of impaired dendritic mrna trafficking |
| topic | BDNF Post-traumatic stress disorder neurotrophins memory deficits hippocampus atrophy dendritic mRNA trafficking |
| url | http://journal.frontiersin.org/Journal/10.3389/fnins.2013.00188/full |
| work_keys_str_mv | AT gabrieleebaj towardsaunifiedbiologicalhypothesisforthebdnfval66metassociatedmemorydeficitsinhumansamodelofimpaireddendriticmrnatrafficking AT davideecarlino towardsaunifiedbiologicalhypothesisforthebdnfval66metassociatedmemorydeficitsinhumansamodelofimpaireddendriticmrnatrafficking AT luciaegardossi towardsaunifiedbiologicalhypothesisforthebdnfval66metassociatedmemorydeficitsinhumansamodelofimpaireddendriticmrnatrafficking AT enricoetongiorgi towardsaunifiedbiologicalhypothesisforthebdnfval66metassociatedmemorydeficitsinhumansamodelofimpaireddendriticmrnatrafficking |