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Figure 4. Illustrative representation of ε, δ and γ PKCs, and RACKs levels in particulate/membrane fractions of rat hippocampus at three different ages, young (Y), middle age (M) and old (O). A different level of ε, δ and γ PKCs in the brain across age may
Figure 10. Figure 4. Illustrative representation of ε, δ and γ PKCs, and RACKs levels in particulate/membrane fractions of rat hippocampus at three different ages, young (Y), middle age (M) and old (O). A different level of ε, δ and γ PKCs in the brain across age may explain the age-related reduction of IPC protection and higher susceptibility of aged brain for cognitive disorders and neurodegeneration. These animal ages reflect a human age of 18, 30/40, and >60 years old, respectively. In the particulate fraction, where activated PKCs translocate, no significance differences were observed in γPKC (blue) and in δPKC (red) expression across the three age groups. However, εPKC (black) levels were lower in the particulate fraction of aged hippocampi compared to the young and middle-aged groups (as represented by the different color intensity, grey). This alteration may explain, at least in part, the greater incidence of AD and damage after cerebral ischemia in elderly individuals (a). The presence of εPKC activators has been demonstrated to restore IPC protection mechanisms in aged brain and to reduce susceptibility to AD and other neurodegenerative diseases where PKCs are involved (b). The red circle with a slash in it represents an inhibitory effect.

विवरण

Schematic representation of PKC isoform and RACK protein distribution in membrane fractions of young versus aged rat hippocampus illustrates the age-dependent loss of neuroprotective mechanisms.

More Figures from This Paper

Subcellular distribution of PKC isoforms between cytosolic and membrane fractions is analyzed, showing altered translocation patterns in aged brain tissue.

Figure 5

Subcellular distribution of PKC isoforms between cytosolic and membrane fractions is analyzed, showing altered translocation patterns in aged brain tissue.

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RACK1 and RACK2 scaffolding protein levels are measured in aging hippocampus, indicating reduced anchoring capacity for activated PKC isoforms.

Figure 6

RACK1 and RACK2 scaffolding protein levels are measured in aging hippocampus, indicating reduced anchoring capacity for activated PKC isoforms.

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Western blot analysis of gamma, delta, and epsilon PKC levels in hippocampus across young, middle-aged, and aged rats demonstrates progressive age-related reduction.

Figure 7

Western blot analysis of gamma, delta, and epsilon PKC levels in hippocampus across young, middle-aged, and aged rats demonstrates progressive age-related reduction.

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Quantitative densitometry of PKC isoform bands confirms statistically significant declines in neuroprotective PKC levels with advancing age.

Figure 8

Quantitative densitometry of PKC isoform bands confirms statistically significant declines in neuroprotective PKC levels with advancing age.

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Activated PKC translocation to membrane fractions is diminished in aged rats, with reduced binding to RACK scaffolding proteins contributing to impaired neuroprotective signaling.

Figure 9

Activated PKC translocation to membrane fractions is diminished in aged rats, with reduced binding to RACK scaffolding proteins contributing to impaired neuroprotective signaling.

chart
RACK1 and RACK2 protein levels in hippocampal tissue are quantified by Western blot across three age groups, with both scaffolding proteins showing age-related reductions.

Figure 11

RACK1 and RACK2 protein levels in hippocampal tissue are quantified by Western blot across three age groups, with both scaffolding proteins showing age-related reductions.

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Figure 10

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Source Paper

Age-Dependent Levels of Protein Kinase Cs in Brain: Reduction of Endogenous Mechanisms of Neuroprotection.

International journal of molecular sciences (2019)

PMID: 31331067

DOI: 10.3390/ijms20143544

Cite This Figure

![Figure 10: Schematic representation of PKC isoform and RACK protein distribution in membrane fractions of young versus aged rat hippocampus illustrates the age-dependent loss of neuroprotective mechanisms.](https://pdfs.citedhealth.com/figures/31331067/140.png)

> Source: Donatella Pastore et al. "Age-Dependent Levels of Protein Kinase Cs in Brain: Reduction of Endogenous Mech." *International journal of molecular sciences*, 2019. PMID: [31331067](https://pubmed.ncbi.nlm.nih.gov/31331067/)
<figure>
  <img src="https://pdfs.citedhealth.com/figures/31331067/140.png" alt="Schematic representation of PKC isoform and RACK protein distribution in membrane fractions of young versus aged rat hippocampus illustrates the age-dependent loss of neuroprotective mechanisms." />
  <figcaption>Figure 10. Schematic representation of PKC isoform and RACK protein distribution in membrane fractions of young versus aged rat hippocampus illustrates the age-dependent loss of neuroprotective mechanisms.<br>  Source: Donatella Pastore et al. "Age-Dependent Levels of Protein Kinase Cs in Brain: Reduction of Endogenous Mech." <em>International journal of molecular sciences</em>, 2019. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/31331067/">31331067</a></figcaption>
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