Age-related loss of phospholipid asymmetry in APP/APP x PS-1/PS-1 human double mutant knock-in mice: Relevance to Alzheimer disease

نویسندگان

  • Miranda L. Bader
  • William R. Markesbery
  • Christa M. Studzinski
  • M. Paul Murphy
  • Allan Butterfield
چکیده

a Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA b Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA c Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536, USA d Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA e Department of Pathology and Neurology, University of Kentucky, Lexington, KY 40536, USA f Department of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY 40536, USA

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Proteomic identification of specifically carbonylated brain proteins in APP(NLh)/APP(NLh) × PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice model of Alzheimer disease as a function of age.

Alzheimer disease (AD) is the most common type of dementia and is characterized pathologically by the presence of neurofibrillary tangles (NFTs), senile plaques (SPs), and loss of synapses. The main component of SP is amyloid-beta peptide (Aβ), a 39 to 43 amino acid peptide, generated by the proteolytic cleavage of amyloid precursor protein (APP) by the action of beta- and gamma-secretases. The...

متن کامل

Potential in vivo amelioration by N-acetyl-L-cysteine of oxidative stress in brain in human double mutant APP/PS-1 knock-in mice: toward therapeutic modulation of mild cognitive impairment.

Alzheimer's disease (AD) is the most prevalent form of dementia among the elderly. Although the underlying cause has yet to be established, numerous data have shown that oxidative stress is implicated in AD as well as in preclinical stages of AD, such as mild cognitive impairment (MCI). The oxidative stress observed in brains of subjects with AD and MCI may be due, either fully or in part, to i...

متن کامل

Oxidative damage in brain from human mutant APP/PS-1 double knock-in mice as a function of age.

Oxidative stress is strongly implicated in the progressive decline of cognition associated with aging and neurodegenerative disorders. In the brain, free radical-mediated oxidative stress plays a critical role in the age-related decline of cellular function as a result of the oxidation of proteins, lipids, and nucleic acids. A number of studies indicate that an increase in protein oxidation and...

متن کامل

Mutations in amyloid precursor protein and presenilin-1 genes increase the basal oxidative stress in murine neuronal cells and lead to increased sensitivity to oxidative stress mediated by amyloid b-peptide (1–42), H2O2 and kainic acid: implications for Alzheimer’s disease

Oxidative stress is observed in Alzheimer’s disease (AD) brain, including protein oxidation and lipid peroxidation. One of the major pathological hallmarks of AD is the brain deposition of amyloid beta-peptide (Ab). This 42-mer peptide is derived from the b-amyloid precursor protein (APP) and is associated with oxidative stress in vitro and in vivo. Mutations in the PS-1 and APP genes, which in...

متن کامل

Proteomic analysis of brain proteins in APP/PS-1 human double mutant knock-in mice with increasing amyloid b-peptide deposition: Insights into the effects of in vivo treatment with N-acetylcysteine as a potential therapeutic intervention in mild cognitive impairment and Alzheimer’s disease

Proteomic analysis of brain proteins in APP/PS-1 human double mutant knock-in mice with increasing amyloid b-peptide deposition: Insights into the effects of in vivo treatment with N-acetylcysteine as a potential therapeutic intervention in mild cognitive impairment and Alzheimer’s disease Renã A. S. Robinson, Gururaj Joshi, Quanzhen Huang, Rukhsana Sultana, Austin S. Baker, Jian Cai, William P...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2010