Carboxyl terminal fragment of beta-amyloid precursor protein: electrophysiological effects and cellular toxicity

• Autorzy: Fraser S. P. , Bryan A.A. , Diss J.K.J. , Kim J.H. , Kim S.H. , Suh Y.H. , Djamgoz M.B.A.
• Języki publikacji: EN

Abstrakty

EN

Alzheimer's disease (AD) is characterized by deposition of β-amyloid (Aβ) in areas of the brain. Aβ is a metabolic fragment of the β-amyloid precursor protein (βAPP). Genetic evidence has linked βAPP to AD, and there is increasing evidence that fragments from βAPP are neurotoxic. Aβ, the main research focus, has been shown to induce depolarizing ion channel activity. Involvement of other cleaved products from βAPP are less clear. We have investigated the 105 amino acid C-terminal peptide (CT105) (containing the full sequence Aβ), an alternative fragment linked with cellular toxicity. CT105 induced non-selective ionic currents in Xenopus oocytes (a model cell used in cell signalling studies) and was toxic to oocytes and mammalian cortical neurones. These results suggest possible involvement of CT105 in inducing the neural toxicity characteristic of AD.

Słowa kluczowe

EN

cortical neuron; beta-amyloid; neuroprotection; Alzheimer's disease; cell toxicity; ion channel formation; toxicity; electrophysiological effect; brain area; oocyte

• Wydawca: -
• Czasopismo: Cellular and Molecular Biology Letters
• Rocznik: 1997
• Tom: 02
• Numer: 2
• Opis fizyczny: p.175-195,fig.

Twórcy

autor

Fraser S. P.

• Imperial College of Science, Technology and Medicine, London, SW7 2BB, UK

autor

Bryan A.A.

autor

Diss J.K.J.

autor

Kim J.H.

autor

Kim S.H.

autor

Suh Y.H.

autor

Djamgoz M.B.A.

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