Neurotrophins, synaptic plasticity and dementia

  title={Neurotrophins, synaptic plasticity and dementia},
  author={Ottavio Arancio and Moses V Chao},
  journal={Current Opinion in Neurobiology},
Brain‐derived neurotrophic factor and the development of structural neuronal connectivity
An overview of the possible actions ofBDNF in the development of neural circuits, with an emphasis on presynaptic actions of BDNF during the structural development of central neurons.
The Neurotrophins and Their Role in Alzheimer’s Disease
The pathology, symptoms and molecular processes associated with Alzheimer’s disease are described and the involvement of the neurotrophins, particularly NGF and BDNF, and their receptors, are discussed, with changes in BDNF considered particularly in the light of its importance in synaptic plasticity.
Brain-Derived Neurotrophic Factor: Linking Fear Learning to Memory Consolidation
The molecular cascade by which fear learning leads to an increase in BDNF expression in the lateral amygdala (LA) is described, which contributes to fear memory consolidation.
Withdrawal of BDNF from hippocampal cultures leads to changes in genes involved in synaptic function
Using a high‐density microarray platform, a significant decrease in genes that are associated with vesicular trafficking and synaptic function are identified, as well as selective increases in MAP kinase phosphatases that are relevant to a wide number of conditions in which levels of BDNF are compromised.
Is Altered BDNF Biosynthesis a General Feature in Patients with Cognitive Dysfunctions?
The hypothesis that abnormalities in proBDNF or mBDNF biosynthesis may correspond to different cognitive dysfunctions in these brain diseases, while the role of truncated BDNF remains unknown is put forward.
Synaptic regulation of affective behaviors; role of BDNF
  • I. Ninan
  • Biology, Psychology
  • 2014


The yin and yang of neurotrophin action
The proteolytic cleavage of proneurotrophins represents a mechanism that controls the direction of action of neurotrophins and has profound implications for the understanding of the role of neurotrophic molecules in a wide range of cellular processes.
Deficits in Synaptic Transmission and Learning in Amyloid Precursor Protein (APP) Transgenic Mice Require C-Terminal Cleavage of APP
In APP transgenic mice with a mutated cleavage site at amino acid 664, normal synaptic transmission, synaptic plasticity, and learning were maintained despite the presence of elevated levels of APP, Aβ42, and even plaque accumulation, indicating that cleavage of APP may play a critical role in the development of synaptic and behavioral dysfunction in APPtransgenic mice.
Single-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor
A model in which postsynaptic depolarization elicits calcium-dependent release of BDNF that diffuses retrogradely and enhances presynaptic transmitter release is confirmed, showing directly at the single-cell level that modulation can occur.
Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment.
It is demonstrated that brief treatment with the phosphodiesterase 4 inhibitor rolipram ameliorates deficits in both long-term potentiation (LTP) and contextual learning in the double-transgenic mice and this beneficial effect can be extended beyond the duration of the administration.
BDNF-mediated neurotransmission relies upon a myosin VI motor complex
An important role is defined for the Myo6-GIPC1 motor complex in presynaptic function and in BDNF-TrkB–mediated synaptic plasticity in postnatal day 12–13 hippocampus.
Activation of p75NTR by proBDNF facilitates hippocampal long-term depression
It is reported that proBDNF, by activating p75NTR, facilitates hippocampal long-term depression (LTD) and the finding that mature BDNF promotes synaptic potentiation, suggest a bidirectional regulation of synaptic plasticity by proBD NF and matureBDNF.