Alzheimer’s and Parkinson’s – conquering the complexities of neuroscience

New neuroscience image

In recent years, research into the nervous system has advanced greatly, thanks to progress in areas like molecular biology, electrophysiology, biochemistry, high-resolution microscopy, computational neuroscience and nanotechnology. We can even understand some complex processes occurring in within a neuron. So nowadays, scientists can study several aspects of the nervous system including how it works, its structure and development, and what happens when it goes wrong. Neurodegeneration is characterized by dysfunction and death of cells in the nervous system. With neurodegenerative diseases such as Parkinson’s and Alzheimer’s, this results in impaired motor function and progressive dementia.

The nervous system is one of the most complex systems within the human body. In fact, approximately 84% of all genes are expressed in the human brain (1). The variety of synapses in the brain is wide and mutations in synaptic genes are associated with numerous brain-related disorders. Therefore, conquering the complexity of neuroscience and understanding its diversity is a key step towards developing specific and effective therapeutics.

Molecular & cellular pathways in neurodegeneration

During the past years, QIAGEN has presented a broad range of webinars related to neuroscience and neurodegeneration to help you understand key aspects of these research areas. Most of them are available online on SlideShare. One of our most viewed webinars – Molecular mechanisms of neurodegeneration: neurodegenerative disorders webinar – focuses on common molecular mechanisms and pathways leading to neurodegeneration, such as Alzheimer’s Disease, Parkinson’s Disease or Multiple Sclerosis. Additionally, we address research and therapeutic strategies as well as how these discoveries and tools can be used to facilitate your neurodegeneration research. Based on different research foci, we have designed downloadable signaling pathway maps as part of our tools and technologies for neuroscience research and various diseases, to better understand the interactions and connections between the genes. Feel free to:

• Visit our Alzheimer’s disease pathway map to understand which mutations in some of the components of the amyloid pathway, such as the amyloid precursor protein APP, ApoE, Presenilin-1 and PS2 (PS1 and Presenilin-2) and SORL1 are responsible for autosomal-dominant early-onset familial Alzheimer disease (FAD) (2)

• Check out the Presenilin-mediated signaling map about mutations which are associated with the occurrence of early-onset familial Alzheimer’s disease. Physiological functions of Presenilins are unknown, but they may be related to developmental signaling, apoptotic signal transduction or processing of selected proteins, such as the Beta-APP (Beta-Amyloid Precursor protein)

• Working with our Parkinson’s disease pathway map will help you to discover proteins and genes associated with Parkinson’s disease, which include alpha-synuclein, Parkin and UCHL1 (Ubiquitin Carboxy-terminal Hydrolase L1), PINK1 (PTEN Induced Kinase-1) and DJ1

I just mentioned a few, but there are hundreds of recent research topics connected to our online tools for neuroscience. One of the latest publications in Basic and Clinical Neuroscience is focusing on gene expression of brain neurotransmitter receptors in mice. In this study, the researchers reported for the first time the alterations in the gene expression of 50 brain neurotransmitter receptors and regulators as quantified using the RT2 PCR Arrays one week after systemic injection of KA (Kainic Acid) in the mice hippocampus. Kainic Acid is commonly used to induce excitotoxicity in animal models of neurodegeneration, which is considered to be a major mechanism of neuronal death in acute and chronic neurodegenerative diseases, such as Alzheimer’s and Parkinson’s (3,4).

To help you overcome the challenges of your Alzheimer’s and Parkinson’s disease research, and take full advantage of the latest genomic technologies, please visit our Neurodegenerative Disease Research Center and look around – you’re sure to find something you need!

 

References 

  1. 1. Allen Institute for Brain Science. (2012, September 19). Human brains share a consistent genetic blueprint and possess enormous biochemical complexity. ScienceDaily. Retrieved March 1, 2017 (link)

2. Mizuno S, Iijima R, Ogishima S, et al. AlzPathway: a comprehensive map of signaling pathways of Alzheimer’s disease. BMC Systems Biology. 2012;6:52. doi:10.1186/1752-0509-6-52 (link)

3. Doble A. The role of excitotoxicity in neurodegenerative disease: implications for therapy. Pharmacology and Therapeutics. 1999;81(3):163–221. doi: 10.1016/s0163-7258(98)00042-4.(link)

4. Sperk G. Kainic acid seizures in the rat. Progress in Neurobiology. 1994;42(1):1–32. doi: 10.1016/0301-0082(94)90019-1 (link)

Laura Alina Mohr, M.Sc.

Laura Alina Mohr joined QIAGEN in 2015. She received her Master’s Degree in Chemical Biology at the Technical University Dortmund in Germany. During this time, she was involved in Systemic Cell Biology research at the prestigious Max Planck Institute. Before joining QIAGEN, Laura Alina worked at the Scripps Research Institute, San Diego, where she first focused on DNA damage/repair pathways and telomere biology. Later, she joined the Muscle Development, Aging and Regeneration program at the Sanford Burnham Prebys Medical Discovery Institute. At QIAGEN she is interested in gene expression profiling focusing on various biological pathways, e.g. cancer research and neurodegeneration.

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