Brain biology is a particularly important subject involved in numerous human maladies. Diseases of the brain, collectively called neurological diseases, can have widespread psychological and biological effects, causing harm to the diseased person and potentially others. Unfortunately, due to the invasive nature of brain biopsy collection, the use of brain tissue specimens is quite prohibitive for the identification of biomarkers for disease stratification. Serum neurological disease biomarkers are much more promising, but have proven elusive. The notable exception being serum Tau levels for early Alzheimer’s detection. Otherwise, neurological disease biomarkers generally revolve around samples taken spinal punctures or brains and spinal cord tissue samples taken postmortem. The limited supply of these sample materials has hampered the ability of current technologies to define novel biomarkers for neurological conditions, in particular for Alzheimer’s and Parkinson’s diseases, complex spectrum disorders such as autism, and neuroinflammation in general.
Recent advances in the field of multiplex cytokine detection now allow for a broad and global view of protein expression in neurological samples in limited supply. Now, rather than being limited to the detection of a handful of proteins, multiplex cytokine arrays offer 20 targets or more, requiring the same amount of sample previously required to detect a single target. Originally developed for non-invasive sample types like serum and plasma, these arrays have now been validated and published with CSF samples, brain tissue lysates, spinal cord samples, as well as numerous in vitro neurological sample types.
RayBiotech’s Neuro Discovery arrays are designed to gather multiple neurologically relevant cytokines together into a broad panel. Covering cytokines involved in cellular communication, inflammation, growth factors and more, our Neuro Discovery Arrays will allow you to maximize your screening of potentially important biomarkers while minimizing the consumption of precious and limited sample supplies.
|Adiponectin (ACRP30)||BDNF||beta-NGF||CNTF||CRP (C-Reactive Protein)|
|Eotaxin-1 (CCL11)||Eotaxin-2 (MPIF-2/CCL24)||Eotaxin-3 (CCL26)||Fas (TNFRSF6/Apo-1)||Fas Ligand (TNFSF6)|
|IFN-gamma||IGF-1||IL-1 alpha (IL-1 F1)||IL-1 beta (IL-1 F2)||IL-10|
|IL-18||IL-4||IL-6||IL-8 (CXCL8)||KC (CXCL1)|
|LIF||LIX||MCP-1 (CCL2)||M-CSF||MIP-1 alpha (CCL3)|
|MIP-1 beta (CCL4)||MMP-2||MMP-3||Neuropilin-1||Notch-1|
|Notch-2||RAGE||S100 B||SDF-1 alpha (CXCL12 alpha)||TARC (CCL17)|
|TGF beta 1||TIMP-1||TNF alpha||VEGF-A|
Adiponectin (APN) is a hormone that is produced and secreted by adipocytes, or fat cells. In this study, Ng et al. demonstrate that APN levels were reduced in the brains of patients with Alzheimer's disease (AD) and 5xFAD mice, which is a mouse model for AD. Moreover, APN deficiency in 5xFAD mice accelerated amyloid loading, increased cerebral amyloid angiopathy, and reduced insulin-signaling activities. Treatment with an APN receptor agonist (AdipoRon) improved neuronal insulin-signaling activities, insulin sensitivity, and spatial memory functions while significantly lowering plaque and cerebral cytokines levels. Their data suggest that chronic adipoRon administration is a potential treatment for AD.
Ng RCL, et al. Chronic oral administration of adipoRon reverses cognitive impairments and ameliorates neuropathology in an Alzheimer's disease mouse model. Molecular Psychiatry (2020). [view publication]
RayBiotech Products: Sandwich ELISA (cat no. ELM-TNFa)
Sample Type: Conditioned medium
Astrocytes help support homeostatic neuronal functions but can become destructive during Alzheimer's disease (AD), a neurodegenerative disease characterized by inflammation. Goetzl et al. measured proinflammatory proteins in astrocyte-derived exosomes (ADEs) from plasma samples of AD patients and matched controls. They found that eleven proteins (of C1q, C4b, C3d, factor B, factor D, Bb, C3b, C5b-C9 terminal complement complex, IL-6, TNFa, IL-1b) were upregulated in ADEs of AD patients compared to controls. Four complement regulatory proteins (CD59, CD46, DAF, complement receptor type 1) were significantly lower for AD patients than controls. This study provides further insight into the AD pathology.
Goetzl EJ, Schwartz JB, Abner EL, Jicha GA, Kapogiannis D. High complement levels in astrocyte-derived exosomes of Alzheimer disease. Ann Neurol (2018). [view publication]
RayBiotech Products: Sandwich ELISA (cat no. ELH-CD59, ELH-IL1b, ELH-MBL)
Sample Type: Plasma-derived exosomes
Peripheral nerve damage causes "neuropathic pain" (NP), a complex chronic condition in which inflammatory mediators are released. To date, no drug is available that is universally effective for NP. Here, the effectiveness of two drug types that modulate pain perception, angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs), to attenuate NP induced by sciatic nerve chronic constriction injury (CCI) in rats was compared to the standard NP treatment. Pain response was assessed in terms of behavior, inflammatory markers, oxidative markers, STAT3 activation, phosphorylation of key proteins, and histopathological findings in the brainstem and sciatic nerve. Their data show that ARBs were superior in improving NP compared to ACE-Is.
Hegazy N, et al. Mechanisms Involved in Superiority of Angiotensin Receptor Blockade over ACE Inhibition in Attenuating Neuropathic Pain Induced in Rats. Neurotherapeutics. (2020). [view publication]
RayBiotech Products: Phosphorylation ELISA (cat no. PEL-Stat3-Y705-T)
Sample Type: Conditioned medium
The molecular mechanisms that drive the progressive loss of dopaminergic (DA) neurons in Parkinson's disease (PD) are not well understood, thus hindering drug development. Using a Drosophila PD model, Maitra et al. show that extensive alteration of innate immune response genes occur in response to paraquat (PQ)-induced oxidative stress prior to symptom onset. PQ treatment also activated Relish, the NF-κB transcription factor, which failed to induce AMP expression that provides protection against Gram-negative bacterial infection. This work demonstrates that environment toxins (i.e., PQ exposure) result in innate immune system modulation, neurodegeneration, and increased susceptibility to bacterial infection.
Maitra U,. et al. Innate immune responses to paraquat exposure in a Drosophila model of Parkinson’s disease. Sci Rep (2019). [view publication]
RayBiotech Products: Antibody (cat no. RB-14-0004)
Species: Drosophila melanogaster (fly)
Sample Type: Tissue lysate
The neuronal regulation of major depressive disorder (MDD) remains elusive. He et al. explored the roles of substance P (SP), the most abundant peptide in the central nervous system and encoded by the Tac1 gene, in MDD. Mice with knocked down Tac1 in the nucleus accumbens (NAc), a brain region with motivation and reward functions, displayed anhedonia-like behavior. Moreover, Tac1NAc-expressing neurons project signals to another critical region of the brain with known reward circuitry, the ventral pallidum (VP). Inactivating a receptor for SP, NK1-R, in the VP ac1 promoted stress susceptibility. This study points to an essential role of Tac1 neurons in regulating depression.
He ZX, et al. Nucleus Accumbens Tac1-Expressing Neurons Mediate Stress-Induced Anhedonia-like Behavior in Mice. Cell Rep. (2020). [view publication]
RayBiotech Products: Competitive ELISA (cat no. EIAM-SP)
Sample Type: Tissue lysate