Increased cerebrospinal fluid levels of transforming growth factor-beta1 in Alzheimer's disease.
Accumulation of beta-amyloid ( Abeta) in senile plaques in specific brain regions is a key event in the development of Alzheimer's disease (AD). Expression of transforming growth factor-beta1 ( TGF-beta1), a regulator of brain responses to inflammation and injury, has been correlated with Abeta accumulation, aggregation and clearance in transgenic mice and increased production of amyloid precursor protein ( APP) followed by Abeta generation in murine and human astrocyte cultures. Here, we compared TGF-beta1 levels in cerebrospinal fluid (CSF) from 20 AD patients and 20 healthy controls and correlated TGF-beta1 to intrathecal levels of the amyloidogenic 42-amino acid fragment of Abeta (Abeta42). AD patients had higher concentration of TGF-beta1 than controls (P = 0.002). Moreover, TGF-beta1 levels were negatively correlated to Abeta42 levels in the whole material (cases and controls, r = -0.35; P = 0.020), although this correlation failed to reach significance in the AD group alone (r = -0.38; P = 0.099). Taken together, the data indicate that TGF-beta1 plays a role in the processes that affect amyloid metabolism in AD.[1]References
- Increased cerebrospinal fluid levels of transforming growth factor-beta1 in Alzheimer's disease. Zetterberg, H., Andreasen, N., Blennow, K. Neurosci. Lett. (2004) [Pubmed]
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