This recent abstract provides evidence for a connection between "Mad Cow" type diseases and AA metabolites:
Int Rev Neurobiol. 2007;82:265-75.
"Cyclooxygenase-2, prostaglandin E2, and microglial activation in
prion diseases."
Cyclooxygenase (COX) catalyzes the first committed step in the
synthesis of prostaglandins (PGs) and is the main target of
nonsteroidal anti-inflammatory drugs (NSAIDs). The enzyme exists as
constitutive (COX-1) and inducible (COX-2) isoforms, being the latter
a major player in inflammation. In the brain, COX-2 expression has
been associated with inflammatory and neurodegenerative processes of
several human neurological diseases. Prion diseases, or transmissible
spongiform encephalopathies, are a heterogeneous group of fatal
neurodegenerative disorders, characterized by deposition of the
protease-resistant prion protein, astrocytosis, and spongiform
degeneration. In addition, an extensive microglial activation supports
the occurrence of local chronic inflammatory response. In experimental
prion diseases, COX-2 immunoreactivity was found specifically
localized to microglial cells and increased with the progression of
disease, along with the number of activated microglia. The induction
of COX-2 was paralleled by a substantial raise in the brain homogenate
PGE(2) levels. In these models, only few scattered COX-1-positive
microglia-like cells were detected, suggesting that COX-2 is the major
form in prion diseases. In line with the animal models, elevated
levels of PGE(2) were found in the cerebrospinal fluid of subjects
affected by sporadic, genetic, or variant CJD. In sporadic CJD
patients, the most numerous group of patients examined, higher CSF
levels of PGE(2) were associated with shorter survival. Although the
mechanisms leading to microglial COX-2 expression as well as its
potential implication in prion disease pathogenesis remain to be
established, PGE(2) levels in the cerebrospinal fluid might represent
an important index to predict survival and disease severity. |
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