Title |
Increased mtDNA mutations with aging promotes amyloid accumulation and brain atrophy in the APP/Ld transgenic mouse model of Alzheimer’s disease
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Published in |
Molecular Neurodegeneration, May 2014
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DOI | 10.1186/1750-1326-9-16 |
Pubmed ID | |
Authors |
Lokesh Kukreja, Gregory C Kujoth, Tomas A Prolla, Fred Van Leuven, Robert Vassar |
Abstract |
The role of mitochondrial dysfunction has long been implicated in age-related brain pathology, including Alzheimer's disease (AD). However, the mechanism by which mitochondrial dysfunction may cause neurodegeneration in AD is unclear. To model mitochondrial dysfunction in vivo, we utilized mice that harbor a knockin mutation that inactivates the proofreading function of mitochondrial DNA polymerase γ (PolgA D257A), so that these mice accumulate mitochondrial DNA mutations with age. PolgA D257A mice develop a myriad of mitochondrial bioenergetic defects and physical phenotypes that mimic premature ageing, with subsequent death around one year of age. |
X Demographics
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United States | 1 | 100% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 1 | 100% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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United States | 1 | 2% |
Germany | 1 | 2% |
Unknown | 64 | 97% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Bachelor | 14 | 21% |
Researcher | 10 | 15% |
Student > Ph. D. Student | 8 | 12% |
Student > Master | 7 | 11% |
Professor > Associate Professor | 4 | 6% |
Other | 10 | 15% |
Unknown | 13 | 20% |
Readers by discipline | Count | As % |
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Biochemistry, Genetics and Molecular Biology | 9 | 14% |
Medicine and Dentistry | 8 | 12% |
Pharmacology, Toxicology and Pharmaceutical Science | 6 | 9% |
Neuroscience | 6 | 9% |
Other | 6 | 9% |
Unknown | 15 | 23% |