disease (AD) is associated with a progressive accumulation of senile plaques
(containing β-amyloid (Aβ)) and neurofibrillary tangles, but the underlying
pathology is still, to a large extent, a mystery. Nevertheless, there is growing
evidence that matrix metalloproteinases (MMPs), molecules produced by neurons and glial
cells, may play an important, but complex, role.
In an article
published last week in Alzheimer’s
Research & Therapy, Stomrud and colleagues examined MMP, tissue inhibitor of
metalloproteinase-1 (TIMP-1), Aβ and
tau protein levels in the cerebrospinal fluid (CSF) of Alzheimer’s patients and
found that compared to individuals with no cognitive dysfunction, AD patients
had higher CSF levels of certain MMPs. Interestingly, cognitively healthy
individuals with risk markers for the future, such as the presence of the APOE-ε4 allele,
also had higher MMP levels when compared to healthy individuals with no risk
results indicate that MMPs could be associated with neuronal degeneration, even
in individuals who are yet to develop any evident cognitive dysfunction.
Very interesting from a professional perspective , also personal perspective – strong family history.
Somehow a finding based on a weak correlation to risk markers in a sub-population of 7 healthy controls does not fill one with confidence in the significance of the results.
Why on earth would anyone have approved this experimental design? It’s not like it would be terribly difficult to get larger sample sizes.
I hope, if this does see publication, the charts will be reformatted to use consistent ranges and domains rather than the arbitrary ones in the preprint.