Repository logo
Communities & Collections
All of DSpace
  • English
  • العربية
  • বাংলা
  • Català
  • Čeština
  • Deutsch
  • Ελληνικά
  • Español
  • Suomi
  • Français
  • Gàidhlig
  • हिंदी
  • Magyar
  • Italiano
  • Қазақ
  • Latviešu
  • Nederlands
  • Polski
  • Português
  • Português do Brasil
  • Srpski (lat)
  • Српски
  • Svenska
  • Türkçe
  • Yкраї́нська
  • Tiếng Việt
Log In
New user? Click here to register.Have you forgotten your password?
  1. Home
  2. Browse by Author

Browsing by Author "Grahame-Smith, D.G."

Filter results by typing the first few letters
Now showing 1 - 1 of 1
  • Results Per Page
  • Sort Options
  • No Thumbnail Available
    Item
    Abnormal functions of pottasium channels in the platelets of patients with Alzheimer's disease
    (Lancet Publishing Group, 1998) de Silva, H.A.; Aronson, J.K.; Grahame-Smith, D.G.; Jobst, K.A.; Smith, A.D.
    BACKGROUND:Reports of abnormalities of potassium-channel function in various cultured cells of Alzheimer's disease patients led us to attempt to characterise the pharmacological characteristics of the abnormal channel.METHODS: We studied platelets from 14 patients with Alzheimer-type dementia and 14 non-demented controls matched for age and sex. The effects of specific inhibitors of K+ channels on the efflux of rubidium-86 ions, a radioactive analogue of K+, from the platelets were measured.FINDINGS: Normal platelets contain three types of K+ channel, sensitive to the inhibitory actions of apamin (small-conductance calcium-dependent potassium channels), charybdotoxin (of less specificity, but probably intermediate-conductance calcium-dependent K+ channels), and alpha-dendrotoxin (voltage-sensitive K+ channels). However, 8Rb+ efflux from the platelets of patients with Alzheimer-type dementia was not inhibited by either apamin or charybdotoxin. By contrast, inhibition by alpha-dendrotoxin did occur. INTERPRETATION: Our results suggest that calcium-dependent K+ channels in platelets are selectively impaired in Alzheimer's disease. A similar abnormality in neurons could contribute to the pathophysiology of the disorder.

DSpace software copyright © 2002-2025 LYRASIS

  • Privacy policy
  • End User Agreement
  • Send Feedback
Repository logo COAR Notify