Overview of Neurodegeneration

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The word neurodegeneration is essentially made up of two words, “neuro,” referring to nerve cells or neurons and “degeneration,” meaning progressive deterioration.  Taken together, neurodegeneration is the loss of neuronal function due to either structural changes1 or cell death2. Neurons are the functional cells of the nervous system, i.e. your brain and spinal cord. Although new neurons are generated throughout a person’s lifetime, the quantity is limited3. When neurons are damaged or die, they cannot rapidly replace themselves4. Neurodegeneration causes a gradual loss of a person’s cognitive abilities, such as memory and decision making2, and is a key trait in the extensive list of neurodegenerative diseases.

While there are hundreds of neurodegenerative diseases with a variety of symptoms and expression, the underlying damage is the same.  The differences in symptoms and disease expression arise from neurodegeneration occurring in different brain areas.  For example, Alzheimer’s disease affects the cortex and hippocampus causing learning and memory deficits5, whereas Parkinson’s disease affects the basal ganglia and results in abnormal movements like tremors and rigidity1. The main risk factor for these neurodegenerative diseases is advanced age6,7.There are some treatments available to alleviate some of the symptoms,  yet none to date can stop or even slow the progression of the neuronal degeneration1.  Furthermore, there is no cure for neurodegeneration.              

Unfortunately, the causes of this debilitating process are virtually unknown.  In some instances where the causes have been identified, the initiation and processes involved are not well understood1. It is estimated that only ~5% of neurodegenerative disease are caused by genetic mutations. The vast majority are thought to be caused by environmental factors, such as an accumulation of toxins within the brain or mitochondrial dysfunction that creates toxic molecules within the neurons1,2.

Despite the lack of understanding in the cause of neurodegeneration, the result is known and leads to cell death. Interestingly, there is mounting evidence that the mode of cell death is quite diverse.  It has been suggested that there are four main types of cell death: apoptotic, necrotic, autophagic and cytoplasmic. The two most widely accepted forms of cell death are apoptosis, or “programmed” cell death in which the cell deliberately commits suicide, and necrotic cell death where the cell membrane ruptures releasing intracellular components into the extracellular space1.

Given that the main risk factor for neurodegeneration and neurodegenerative diseases is age, the incidences of these diseases are becoming more frequent as the population ages. As the disease rate increases, it costs the world billions of dollars in healthcare expenditures and lost economic productivity6.

Continued research on the genetics, causes, symptoms and initiation of neurodegeneration is necessary to develop novel disease modifying treatments or interventions that produce a long lasting change and/or delay in disease progression.


Detection of mouse IP3R1 (red) in FFPE cerebellum by IHC-IF

Detection of mouse IP3R1 (red) in FFPE cerebellum by IHC-IF. Antibody: Rabbit anti-IP3R1 (A302-158A). Secondary: DyLight® 594-conjugated goat anti-rabbit IgG (A120-201D4). Counterstain: DAPI (blue).

Detection of mouse IP3R1 in FFPE cerebellum by IHC

Detection of mouse IP3R1 in FFPE cerebellum by IHC. Antibody: Rabbit anti-IP3R1 (A302-158A). Secondary: HRP-conjugated goat anti-rabbit IgG (A120-501P). Substrate: DAB.

Detection of mouse Lamin-A/C (green) in FFPE brain (hippocampus CA3 region) by IHC-IF

Detection of mouse Lamin-A/C (green) in FFPE brain (hippocampus CA3 region) by IHC-IF. Antibody: Affinity purified rabbit anti-Lamin-A/C (A303-430A). Secondary: DyLight® 488-conjugated goat anti-rabbit IgG (A120-201D2). Counterstain: DAPI (blue).


Below is the entire list of targets involved in neurodegeneration research. Can’t find what you are looking for? Bethyl offers a custom antibody service.




1. Przedborski S, Vila M, Jackson-Lewis V. 2003. Neurodegeneration: what is it and where are we?. J. Clin. Invest. Jan 1;111(1):3-10.

2. OBI (Ontario Brain Institute), 2015. Brainnovation snapshot [Internet]. [Cited 12 Nov 2017]. Available from http://archive.braininstitute.ca/sites/default/files/neurodegeneration_brainnovation_final.pdf

3. Knobloch M and Jessberger S. 2011. Perspectives on adult neurogenesis. Eur J Neurosci. Mar;33(6):1013-1017.

4. JPND (EU Joint Programme-Neurodegenerative Disease Research), 2017. What is neurodegenerative disease? [Internet]. [Cited 12 Nov 2017.] Available from http://www.neurodegenerationresearch.eu/about/what/

5. Jeong S. 2017. Molecular and cellular basis of neurodegeneration in Alzheimer’s disease. Mol Cells. Sep 30;40(9):613-620.

6. Cummings J. 2017. Disease modification and neuroprotection in neurodegenerative disorders. Transl Neurodegener. 6:25.

7. Salvadores N, Sanhueza M, Mangue P, Court FA. 2017. Axonal degeneration during aging and its functional role in neurodegenerative disorders. Front Neurosci. Sept 4;11:451.