Abstract
Background Disruption of CNS microvessels and CSF-bordering cells (ependyma, choroid plexus and leptomeninges) can alter fluid flow among the CNS compartments. This leads to hydrocephalus. An excess of basic fibroblast growth factor (FGF2) or amyloid precursor protein (APP), from which A-Beta fragments derive, predisposes to altered fluid dynamics and amyloid retention. We combined these risk factors to accelerate development of hydrocephalus. Hypothesis: Doubly-transgenic animals, overexpressed for FGF2 and APP, have greater morbidity in respect to compromised CSF turnover and toxic A-Beta effects. We also postulated CSF/brain and blood/brain interfaces to be especially vulnerable in double overexpression.
Highlights
Disruption of CNS microvessels and CSF-bordering cells can alter fluid flow among the CNS compartments
52nd Annual Meeting of the Society for Research into Hydrocephalus and Spina Bifida Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here.
We postulated CSF/brain and blood/brain interfaces to be especially vulnerable in double overexpression
Summary
Altered ependyma and leptomeninges in transgenic mice that over express FGF2 and amyloid precursor protein: evidence for early hydrocephalus. Edward Stopa*1, Miles Miller, Eddie Blay, Paul McMillan, Douglas Coffin, Andrew Baird, John Donahue and Conrad Johanson. Address: 1Neuropatholgy and Clinical Neuroscience, Brown Medical School, Providence, Rhode Island 02903, USA, 2Montana Cancer Institute Foundation, University of Montana, Missoula, MT, USA and 3Pharmacy School, University of California San Diego, San Diego, CA, USA. Published: 3 February 2009 Cerebrospinal Fluid Research 2009, 6(Suppl 1):S4 doi:10.1186/1743-8454-6-S1-S4. 52nd Annual Meeting of the Society for Research into Hydrocephalus and Spina Bifida Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here.
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