Related Experiment Video
Updated: Apr 6, 2026
08:33
Characterizing Histone Post-translational Modification Alterations in Yeast Neurodegenerative Proteinopathy Models
Published on: March 24, 2019
8.0K
Poly(ADP-ribosylation) and neurodegenerative disorders
Davide Alessandro Basello1, Anna Ivana Scovassi1
1Istituto di Genetica Molecolare CNR, Via Abbiategrasso 207, 27100 Pavia, Italy.
Mitochondrion
|July 22, 2015
Summary
Impaired mitochondria are key in neurodegeneration. Poly(ADP-ribosylation) activation signals cell death, but inhibitors may offer therapeutic potential for these debilitating brain disorders.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Neurodegenerative disorders exhibit compromised mitochondrial structure and function.
- Neural cell death in these conditions is triggered by unknown signaling pathways.
- Poly(ADP-ribosylation) is a protein modification implicated in cell death signaling.
Purpose of the Study:
- To describe the fundamental characteristics of poly(ADP-ribosylation).
- To focus on the role of poly(ADP-ribosylation) in mitochondrial events.
- To explore the potential of poly(ADP-ribosylation) inhibitors in neurodegenerative disease treatment.
Main Methods:
- Review of existing literature on poly(ADP-ribosylation) and neurodegeneration.
- Analysis of mitochondrial roles in cell death pathways.
- Illustration of cell death paradigms including apoptosis, parthanatos, necroptosis, and mitophagy.
Main Results:
- Poly(ADP-ribosylation) produces poly(ADP-ribose), a signaling molecule.
- This process is linked to various cell death mechanisms.
- Mitochondrial dysfunction is a central aspect of these pathways.
Conclusions:
- Poly(ADP-ribosylation) plays a significant role in neurodegenerative processes.
- Targeting poly(ADP-ribosylation) with inhibitors presents a promising therapeutic strategy.
- Further research into poly(ADP-ribosylation) inhibitors could lead to novel treatments for neurodegeneration.
Related Concept Videos
01:26Alzheimer's Disease: Overview
2.0K
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
2.0K
01:15Parkinson's Disease: Overview
2.4K
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
2.4K
02:23RNA Editing
10.2K
RNA editing is a post-transcriptional modification where a precursor mRNA (pre-mRNA) nucleotide sequence is changed by base insertion, deletion, or modification. The extent of RNA editing varies from a few hundred bases, in mitochondrial DNA of trypanosomes, to a just single base, in nuclear genes of mammals. Even a single base change in the pre-mRNA can convert a codon for one amino acid into the codon for another amino acid or a stop codon. This type of re-coding can significantly affect the...
10.2K
01:37Neural Regulation
44.9K
Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
44.9K
03:03Amyloid Fibrils
13.1K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
13.1K
01:28Biosynthesis of Nucleic Acids
1.6K
Nucleic acid biosynthesis is a fundamental biochemical process that produces the purine and pyrimidine nucleotides essential for DNA and RNA synthesis. This pathway maintains a balanced nucleotide pool, preventing imbalances that could jeopardize genetic integrity and cellular function. Given the crucial role of nucleotides, their synthesis is tightly regulated to ensure proper cellular homeostasis.Purine BiosynthesisThe biosynthesis of purine nucleotides begins with ribose-5-phosphate, a...
1.6K