NSE and TUJ-1 and Parkinson's Disease Research

I would like to thank Meghan Coakley from University College Cork for alerting me to a new publication referencing our Chicken NSE (Neuron-Specific Enolase) and Tuj 1 (Neuron-specific class III beta-tubulin) antibodies.

Here's her feedback: "Just letting you know we published our paper using the beta-III-Tubulin and NSE antibodies you supplied to us – Timmons et al., Neuroscience Letters, Oct 1, 2009 [Epub ahead of print]. The antibodies were excellent and I’m sure we’ll be using Neuromics again in the future."

Timmons S, Coakley MF, Moloney AM, O' Neill C. Akt signal transduction dysfunction in Parkinson's disease. Neurosci Lett. 2009 Oct 1. [Epub ahead of print].

Abstract: Significant attention has been drawn to the potential role of defective PI3-kinase-Akt (PKB) signalling in Parkinson's disease (PD) neurodegeneration and to the possibility that activation of Akt may provide neuroprotection in PD. However, little knowledge exists on the integrity of the Akt system in PD. Results of the present study show diminished levels of both total and active phospho(Ser473)-Akt in the brain in PD. This was evident by western blot analysis of midbrain fractions from PD compared to non-PD control brain, but more specifically by immunofluorescence microscopy of the substantia nigra pars compacta (SNpc). Here, double immunofluorescence microscopy found Akt and phospho(Ser473)-Akt to be expressed at high levels in tyrosine hydroxylase (TH) immunopositive dopaminergic neurons in control human brain. Selective loss of these neurons was accompanied by a marked decrease of Akt and phospho(Ser473)-Akt expression in the PD brain, however Akt and active phospho(Ser473)-Akt are still evident in degenerating dopaminergic neurons in the disease. This suggests that it may be possible to target neuronal Akt in advanced PD. Converse to the marked loss of neuronal Akt in PD, increased Akt and phospho(Ser473)-Akt levels were observed in small non-TH positive cells in PD SNpc, whose increased number and small nuclear size indicate they are glia. These findings implicate defective Akt as a putative signalling pathway linked to loss of dopaminergic neurons in PD.

Other Reagents to Consider:
Tuj 1 (Neuron-specific class III beta-tubulin)-Mouse Monoclonal
Neuron/Glial Marker Antibodies
Neurotrophins-Neuron/Glial Marker Proteins
Neurodegenerative Disease Research Antibodies
Neurodegenerative Disease Research Proteins
Stem Cell Research Reagents

More Success with TRPV1

Dr. Irmgard Tegeder and team have been using our VR1 N-Terminus (TRPV1) as a marker to study how B kinase (IKK) plays a role in sensory neuron excitability and nociception.

The antibody was used for both Western Blot and Immunohistochemistry. Here's a recent publication of their results:

Vanessa Bockhart, Cristina Elena Constantin, Annett Häussler, Nina Wijnvoord, Maike Kanngiesser, Thekla Myrczek, Geethanjali Pickert,Laura Popp, Jürgen-Markus Sobotzik, Manolis Pasparakis, Rohini Kuner, Gerd Geisslinger, Christian Schultz, Michaela Kress, and Irmgard Tegeder. Inhibitor B Kinase β Deficiency in Primary Nociceptive Neurons Increases TRP Channel Sensitivity. The Journal of Neuroscience, October 14, 2009, 29(41):12919-12929; doi:10.1523/JNEUROSCI.1496-09.2009

Related Reagents:
All TRPV (Vanilloid); TRPM; TRPA and TRPC Antibodies
Pain and Inflammation Research Antibodies

MMP-9 Squared

We are feverishly working on adding reagents for studying Autoimmunity and Immune Response. In this context, we wanted to alert you to 2 new publications referencing our Matrix Metalloproteinase 9 (MMP-9) antibody.

Zhi-Yuan Zhang, Zhiren Zhang, Caroline Zug, Barbara Nuesslein-Hildesheim, David Leppert and Hermann J. Schluesener. AUY954, a selective S1P1 modulator, prevents experimental autoimmune neuritis. doi:10.1016/j.jneuroim.2009.09.010.

Abstract:
Experimental autoimmune neuritis (EAN) is a T cell-mediated autoimmune inflammatory demyelinating disease of the peripheral nervous system and an animal model of human inflammatory demyelinating polyradiculoneuropathy. AUY954, which targets selectively the sphingosine-1-phosphate receptor 1 (S1P1), is known to sequester lymphocytes into secondary lymphoid tissues. In EAN rats, AUY954 greatly prevented paraparesis if administrated from the day of immunization. T cell, B cell, and macrophage infiltration, inflammatory demyelination, and local expression of interleukine-17 and matrix metalloproteinase-9 in sciatic nerves of EAN rats were significantly decreased by AUY954 treatment. Therefore, S1P1 modulation might be a potential treatment option for inflammatory neuropathies.

Image: MMP-9 expression in the sciatic nerves of control (A) vs AUY954 (B) treated rats.

Yasuki Yasuda, Yoko Matsumura, Kazuki Kasahara, Noriko Ouji, Shigeki Sugiura, Keiichi Mikasa, and Eiji Kita. Microbial exposure early in life regulates airway inflammation in mice after infection with Streptococcus pneumoniae with enhancement of local resistance. Am J Physiol Lung Cell Mol Physiol, Sep 2009; doi:10.1152/ajplung.00193.2009

...with 10% milk in TBST (10mM Tris, 0.15M NaCl, 0.1% Tween-20), followed by probing with goat anti-mouse MMP-9 antibodies (Ab) (Neuromics Antibodies, Edina, MN, GT15020; 1:5000)...

Related Reagents:

CaMKIIs
CD and Cell Surface Markers
ERKs/MAPKs
Heat Shock Proteins-New
Matrix Metalloproteinases (MMPs)
ILs, CCRs, CXCs and STATs
Wnts/FZDs
Other Immune Response Antibodies

Immune Response Research Proteins

Apoptosis Research Reagents