Alternative Splicing in Alzheimer’s Disease
Neurodegenerative diseases have a variety of different genes contributing to their underlying pathology. Unfortunately, for many of these diseases it is not clear how changes in gene expression affect pathology. Transcriptome analysis of neurodegenerative diseases using ribonucleic acid sequencing (...
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| Format: | Online |
| Language: | English |
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2015
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772657/ |
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pubmed-47726572016-03-01 Alternative Splicing in Alzheimer’s Disease Love, Julia E. Hayden, Eric J. Rohn, Troy T. Article Neurodegenerative diseases have a variety of different genes contributing to their underlying pathology. Unfortunately, for many of these diseases it is not clear how changes in gene expression affect pathology. Transcriptome analysis of neurodegenerative diseases using ribonucleic acid sequencing (RNA Seq) and real time quantitative polymerase chain reaction (RT-qPCR) provides for a platform to allow investigators to determine the contribution of various genes to the disease phenotype. In Alzheimer’s disease (AD) there are several candidate genes reported that may be associated with the underlying pathology and are, in addition, alternatively spliced. Thus, AD is an ideal disease to examine how alternative splicing may affect pathology. In this context, genes of particular interest to AD pathology include the amyloid precursor protein (APP), TAU, and apolipoprotein E (APOE). Here, we review the evidence of alternative splicing of these genes in normal and AD patients, and recent therapeutic approaches to control splicing. 2015-08-15 2015-08 /pmc/articles/PMC4772657/ /pubmed/26942228 http://dx.doi.org/10.13188/2376-922X.1000010 Text en http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Love, Julia E. Hayden, Eric J. Rohn, Troy T. |
| spellingShingle |
Love, Julia E. Hayden, Eric J. Rohn, Troy T. Alternative Splicing in Alzheimer’s Disease |
| author_facet |
Love, Julia E. Hayden, Eric J. Rohn, Troy T. |
| author_sort |
Love, Julia E. |
| title |
Alternative Splicing in Alzheimer’s Disease |
| title_short |
Alternative Splicing in Alzheimer’s Disease |
| title_full |
Alternative Splicing in Alzheimer’s Disease |
| title_fullStr |
Alternative Splicing in Alzheimer’s Disease |
| title_full_unstemmed |
Alternative Splicing in Alzheimer’s Disease |
| title_sort |
alternative splicing in alzheimer’s disease |
| description |
Neurodegenerative diseases have a variety of different genes contributing
to their underlying pathology. Unfortunately, for many of these diseases it is
not clear how changes in gene expression affect pathology. Transcriptome
analysis of neurodegenerative diseases using ribonucleic acid sequencing (RNA
Seq) and real time quantitative polymerase chain reaction (RT-qPCR) provides for
a platform to allow investigators to determine the contribution of various genes
to the disease phenotype. In Alzheimer’s disease (AD) there are several
candidate genes reported that may be associated with the underlying pathology
and are, in addition, alternatively spliced. Thus, AD is an ideal disease to
examine how alternative splicing may affect pathology. In this context, genes of
particular interest to AD pathology include the amyloid precursor protein
(APP), TAU, and apolipoprotein E
(APOE). Here, we review the evidence of alternative
splicing of these genes in normal and AD patients, and recent therapeutic
approaches to control splicing. |
| publishDate |
2015 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772657/ |
| _version_ |
1613545369549930496 |