Inhibition of NF-kappa B potentiates amyloid beta-mediated neuronal apoptosis

Kaltschmidt B, Uherek M, Wellmann H, Volk B, Kaltschmidt C (1999)
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 96(16): 9409-9414.

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Autor*in
Kaltschmidt, BarbaraUniBi; Uherek, M.; Wellmann, H.; Volk, B.; Kaltschmidt, ChristianUniBi
Abstract / Bemerkung
One mechanism leading to neurodegeneration during Alzheimer's disease (AD) is amyloid beta peptide (A beta) neurotoxicity. A beta elicits in cultured central nervous system neurons a biphasic response: a low-dose neurotrophic response and a high-dose neurotoxic response. Previously me reported that NF-kappa B is activated by low doses of A beta only. Here we show that NF-kappa B activation leads to neuroprotection. In primary neurons me found that a pretreatment with 0.1 mu M A beta-(1-40) protects against neuronal death induced with 10 mu M A beta-(1-40). As a known neuroprotective agent we nest analyzed the effect of tumor necrosis factor alpha (TNF-alpha). Maximal activation of NF-kappa B was found with 2 ng/ml TNF-alpha. Pretreatment with TNF-alpha protected cerebellar granule cells from tell death induced by 10 mu M A beta-(1-40). This protection is described by an inverted U-shaped dose response and is maximal with a NF-kappa B-activating dose. The molecular specificity of this protective effect was analyzed by specific blockade of NF-kappa B activation. Overexpression of a transdominant negative I kappa B-alpha blocks NF-kappa B activation and potentiates A beta-mediated neuronal apoptosis. Our findings show that activation of NF-kappa B is the underlying mechanism of the neuroprotective effect of low-dose A beta and TNF-alpha. In accordance with these in vitro data we find that nuclear NF-kappa B immunoreactivity around various plaque stages of AD patients is reduced in comparison to age-matched controls, Taken together these data suggest that pharmacological NF-kappa B activation may be a useful approach in the treatment of AD and related neurodegenerative disorders.
Erscheinungsjahr
1999
Zeitschriftentitel
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Band
96
Ausgabe
16
Seite(n)
9409-9414
ISSN
0027-8424
eISSN
1091-6490
Page URI
https://pub.uni-bielefeld.de/record/2462132

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Kaltschmidt B, Uherek M, Wellmann H, Volk B, Kaltschmidt C. Inhibition of NF-kappa B potentiates amyloid beta-mediated neuronal apoptosis. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 1999;96(16):9409-9414.
Kaltschmidt, B., Uherek, M., Wellmann, H., Volk, B., & Kaltschmidt, C. (1999). Inhibition of NF-kappa B potentiates amyloid beta-mediated neuronal apoptosis. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 96(16), 9409-9414. doi:10.1073/pnas.96.16.9409
Kaltschmidt, B., Uherek, M., Wellmann, H., Volk, B., and Kaltschmidt, C. (1999). Inhibition of NF-kappa B potentiates amyloid beta-mediated neuronal apoptosis. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 96, 9409-9414.
Kaltschmidt, B., et al., 1999. Inhibition of NF-kappa B potentiates amyloid beta-mediated neuronal apoptosis. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 96(16), p 9409-9414.
B. Kaltschmidt, et al., “Inhibition of NF-kappa B potentiates amyloid beta-mediated neuronal apoptosis”, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, vol. 96, 1999, pp. 9409-9414.
Kaltschmidt, B., Uherek, M., Wellmann, H., Volk, B., Kaltschmidt, C.: Inhibition of NF-kappa B potentiates amyloid beta-mediated neuronal apoptosis. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 96, 9409-9414 (1999).
Kaltschmidt, Barbara, Uherek, M., Wellmann, H., Volk, B., and Kaltschmidt, Christian. “Inhibition of NF-kappa B potentiates amyloid beta-mediated neuronal apoptosis”. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 96.16 (1999): 9409-9414.

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Control of apoptosis by Rel/NF-kappaB transcription factors.
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