Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease

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Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease. / Diaz, Ricardo Gredilla; Weissman, Lior; Yang, Jenq-Lin; Bohr, Vilhelm A; Stevnsner, Tinna V.

In: Neurobiology of Aging, 12.08.2010.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Diaz, RG, Weissman, L, Yang, J-L, Bohr, VA & Stevnsner, TV 2010, 'Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease', Neurobiology of Aging. https://doi.org/10.1016/j.neurobiolaging.2010.06.019

APA

Diaz, R. G., Weissman, L., Yang, J-L., Bohr, V. A., & Stevnsner, T. V. (2010). Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease. Neurobiology of Aging. https://doi.org/10.1016/j.neurobiolaging.2010.06.019

Vancouver

Diaz RG, Weissman L, Yang J-L, Bohr VA, Stevnsner TV. Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease. Neurobiology of Aging. 2010 Aug 12. https://doi.org/10.1016/j.neurobiolaging.2010.06.019

Author

Diaz, Ricardo Gredilla ; Weissman, Lior ; Yang, Jenq-Lin ; Bohr, Vilhelm A ; Stevnsner, Tinna V. / Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease. In: Neurobiology of Aging. 2010.

Bibtex

@article{199c87610af14b10acdedd8befbfd915,

title = "Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease",

abstract = "Brain aging is associated with synaptic decline and synaptic function is highly dependent on mitochondria. Increased levels of oxidative DNA base damage and accumulation of mitochondrial DNA (mtDNA) mutations or deletions lead to mitochondrial dysfunction, playing an important role in the aging process and the pathogenesis of several neurodegenerative diseases. Here we have investigated the repair of oxidative base damage, in synaptosomes of mouse brain during normal aging and in an AD model. During normal aging, a reduction in the base excision repair (BER) capacity was observed in the synaptosomal fraction, which was associated with a decrease in the level of BER proteins. However, we did not observe changes between the synaptosomal BER activities of presymptomatic and symptomatic AD mice harboring mutated amyolid precursor protein (APP), Tau, and presinilin-1 (PS1) (3xTgAD). Our findings suggest that the age-related reduction in BER capacity in the synaptosomal fraction might contribute to mitochondrial and synaptic dysfunction during aging. The development of AD-like pathology in the 3xTgAD mouse model was, however, not associated with deficiencies of the BER mechanisms in the synaptosomal fraction when the whole brain was analyzed.",

author = "Diaz, {Ricardo Gredilla} and Lior Weissman and Jenq-Lin Yang and Bohr, {Vilhelm A} and Stevnsner, {Tinna V.}",

year = "2010",

month = aug,

day = "12",

doi = "10.1016/j.neurobiolaging.2010.06.019",

language = "English",

journal = "Neurobiology of Aging",

issn = "0197-4580",

publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Mitochondrial base excision repair in mouse synaptosomes during normal aging and in a model of Alzheimer's disease

AU - Diaz, Ricardo Gredilla

AU - Weissman, Lior

AU - Yang, Jenq-Lin

AU - Bohr, Vilhelm A

AU - Stevnsner, Tinna V.

PY - 2010/8/12

Y1 - 2010/8/12

N2 - Brain aging is associated with synaptic decline and synaptic function is highly dependent on mitochondria. Increased levels of oxidative DNA base damage and accumulation of mitochondrial DNA (mtDNA) mutations or deletions lead to mitochondrial dysfunction, playing an important role in the aging process and the pathogenesis of several neurodegenerative diseases. Here we have investigated the repair of oxidative base damage, in synaptosomes of mouse brain during normal aging and in an AD model. During normal aging, a reduction in the base excision repair (BER) capacity was observed in the synaptosomal fraction, which was associated with a decrease in the level of BER proteins. However, we did not observe changes between the synaptosomal BER activities of presymptomatic and symptomatic AD mice harboring mutated amyolid precursor protein (APP), Tau, and presinilin-1 (PS1) (3xTgAD). Our findings suggest that the age-related reduction in BER capacity in the synaptosomal fraction might contribute to mitochondrial and synaptic dysfunction during aging. The development of AD-like pathology in the 3xTgAD mouse model was, however, not associated with deficiencies of the BER mechanisms in the synaptosomal fraction when the whole brain was analyzed.

AB - Brain aging is associated with synaptic decline and synaptic function is highly dependent on mitochondria. Increased levels of oxidative DNA base damage and accumulation of mitochondrial DNA (mtDNA) mutations or deletions lead to mitochondrial dysfunction, playing an important role in the aging process and the pathogenesis of several neurodegenerative diseases. Here we have investigated the repair of oxidative base damage, in synaptosomes of mouse brain during normal aging and in an AD model. During normal aging, a reduction in the base excision repair (BER) capacity was observed in the synaptosomal fraction, which was associated with a decrease in the level of BER proteins. However, we did not observe changes between the synaptosomal BER activities of presymptomatic and symptomatic AD mice harboring mutated amyolid precursor protein (APP), Tau, and presinilin-1 (PS1) (3xTgAD). Our findings suggest that the age-related reduction in BER capacity in the synaptosomal fraction might contribute to mitochondrial and synaptic dysfunction during aging. The development of AD-like pathology in the 3xTgAD mouse model was, however, not associated with deficiencies of the BER mechanisms in the synaptosomal fraction when the whole brain was analyzed.

U2 - 10.1016/j.neurobiolaging.2010.06.019

DO - 10.1016/j.neurobiolaging.2010.06.019

M3 - Journal article

C2 - 20708822

JO - Neurobiology of Aging

JF - Neurobiology of Aging

SN - 0197-4580

ER -

ID: 33492118