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Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Interactions Between Signaling Pathways01:19

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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Microtubule Associated Proteins (MAPs)01:42

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Microtubule function and architecture are regulated by an array of specialized proteins called microtubule-associated proteins or MAPs. These proteins are widespread across different organisms and have conserved protein motifs, like the multi-TOG domain for tubulin binding found in the CLASP family of MAPs. Some MAPs are lineage-specific based on their conserved domains. Their functions depend upon the cytoskeletal architecture and cell type they are located within. In-plant cells, a specific...
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Integration of Synaptic Events01:28

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Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
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Postsynaptic Potential (PSP)01:32

Postsynaptic Potential (PSP)

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Postsynaptic potential (PSP) refers to a change in the electrical potential of a neuron when neurotransmitters released by presynaptic neurons bind to postsynaptic receptors. This potential can either be excitatory, leading to depolarization and ultimately action potential generation, or inhibitory, leading to hyperpolarization and suppression of the postsynaptic neuron.
There are two types of receptors: ionotropic and metabotropic.
The ionotropic receptor is the membrane protein that has an...
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cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Related Experiment Video

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Involvement of p38 MAPK in Synaptic Function and Dysfunction.

Chiara Falcicchia1, Francesca Tozzi2, Ottavio Arancio3

  • 1Institute of Neuroscience, Italian National Research Council, 56124 Pisa, Italy.

International Journal of Molecular Sciences
|August 13, 2020
PubMed
Summary
This summary is machine-generated.

p38 mitogen-activated protein kinase (MAPK) influences neuronal plasticity and Alzheimer's disease (AD) pathology. Inhibiting the p38 MAPK alpha isoform shows promise for treating AD-related synaptic and memory deficits in mouse models.

Keywords:
Alzheimer’s diseaseTauneuroinflammationp38-MAPK α inhibitorsynaptic plasticityβ-amyloid

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • p38 MAPK is crucial for neuronal plasticity, including long-term potentiation (LTP) and long-term depression (LTD).
  • p38 MAPK is activated by stress and neuroinflammation, and implicated in Alzheimer's disease (AD) pathophysiology due to amyloid-beta (Aβ) peptides and tauopathies.

Purpose of the Study:

  • To elucidate the role of p38 MAPK in synaptic plasticity.
  • To investigate the therapeutic potential of targeting p38 MAPK in a neurodegeneration animal model.

Main Methods:

  • Review of existing literature on p38 MAPK in neuronal plasticity and AD.
  • Analysis of findings from animal models of neurodegeneration, specifically AD mouse models.

Main Results:

  • p38 MAPK signaling is activated by Aβ and tau pathologies in AD.
  • Specific inhibitors of the p38 MAPK alpha isoform have demonstrated efficacy in improving synaptic and memory deficits in AD mouse models.

Conclusions:

  • The p38 MAPK pathway is a key regulator of synaptic plasticity and is dysregulated in Alzheimer's disease.
  • Targeting the p38 MAPK alpha isoform represents a promising neurotherapeutic strategy for ameliorating cognitive impairments in AD.