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 β-peptide (1-42), H₂O₂ and kainic acid: Implications for Alzheimer's disease

Hafiz Mohmmad Abdul, Rukhsana Sultana, Jeffrey N. Keller, Daret K. St. Clair, William R. Markesbery, D. Allan Butterfield

Toxicology and Cancer Biology
Markey Cancer Center / Cancer Research Priority Initiative
Chemistry
Office of the Vice President for Research

Research output: Contribution to journal › Article › peer-review

111 Scopus citations

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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 β-peptide (1-42), H2O2 and kainic acid: Implications for Alzheimer's disease

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Neuroscience

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 β-peptide (1-42), H₂O₂ and kainic acid: Implications for Alzheimer's disease