Sunday, August 16, 2009

Link Between Inflammation and Tau Pathology in Alzheimer's Disease

Providing reagents for Alzheimer's Disease Researchers is a strategic focus area for us. This includes making a variety of Primary Neuronal Cultures available to these researchers.

We evolve the strategy based on Researcher input and how the cultures are being referenced in publications. This reference is especially satisfying because of the vangaurd findings:

Lisette T. Arnaud, Natura Myeku and Maria E. Figueiredo-Pereira. Proteasome–caspase–cathepsin sequence leading to tau pathology induced by prostaglandin J2 in neuronal cells. Journal of Neurochemistry. Volume 110 Issue 1, Pages 328 - 342.

"Our data suggest a potential sequence of events triggered by the neurotoxic product of inflammation PGJ2 leading to tau pathology. The accumulation of Ub proteins is an early response. If cells fail to overcome the toxic effects induced by PGJ2, including accumulation of Ub proteins, apoptosis kicks in triggering caspase activation and tau cleavage, the clearance of which by cathepsins could be compromised culminating in tau pathology. Our studies are the first to provide a mechanistic link between inflammation and tau pathology."

Featured Reagent:
E18 Primary Rat Cortical Neurons

Related Reagents:

Images: Neural phenotypes derived from hN2 cell lines. (A) Phase contrast image of differentiated culture. (B) Network including post-mitotic motoneurons (HB9). (C) Cholinergic neuron. (D) Tuj-1 positive cells that are DAT-positive (dopamine transporter; closed arrow) and DAT-negative (open arrow). (E) Gabaergic neurons, inset illustrates GABA in axon, but not the dendrites (arrow).
We will continue to post "whats new" in AD research and potential uses of our reagents.

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