The neuropsychological topic that I chose to investigate was neurodegenerative diseases. Because of the heavily medical and biological nature of this subject I did a little bit of basic background research in order to better understand the nature of the diseases and the primary research papers.
Firstly, neurodegeneration is the progressive loss of structure and function of neurons including the death of neurons. Common neurodegenerative diseases include Parkinson’s, Alzheimer’s and Huntington’s. On a very biological level, many neurodegenerative diseases are caused by genetic mutations, specifically the repeat of a CAG nucleotide triplet. This nucleotide triplet encodes for the amino acid glutamine, thus diseases caused by this genetic mutation are known as polyglutamine diseases. There are nine inherited neurodegenerative polyglutamine diseases including Huntington’s. Similarly, Parkinson’s is caused by abnormal aggregates of proteins as well; these aggregates are known as Lewy bodies and develop inside nerve cells. Diseases caused by the accumulation of intracellular toxic proteins that lead to the eventual degeneration of neurons are categorized as proteinopathies. Many other neurodegenerative diseases are caused by neuron death. The most common form of cell death in neurodegeneration is through mitochondrial dysfunction resulting in apoptosis. Reactive oxygen species (ROS) are normal byproducts of mitochondrial activity but when there is mitochondrial dysfunction over production of ROS occurs resulting in oxidative stress, a central feature of all neurodegenerative disorders. Thus it is very likely that mitochondrial dysfunction and oxidative stress play a largely causal role in neurodegenerative diseases. Lin and Beal (2006) conducted research on the relationship between ROS and neurodegeneration. Finally, the greatest risk factor for neurodegenerative diseases is aging. Many neurodegenerative diseases are late-onset which indicates there is some factor that changes with aging; in each disease neurons gradually lose function as the disease progresses with age.
On a medical level, protein degradation treatments are being studied heavily; recent research by Rubinsztein (2006) studies the roles of intracellular protein-degradation pathways in neurodegeneration. The treatments involve helping to prevent the synthesis of irregular proteins and the process which leads to eventual degradation of neurons but involve very complex pathways that are only beginning to be understood. There is also research by Brody and Holtzman (2008) involving immunotherapy in order to enhance the innate immune system against Alzheimer’s.
As far as research on treatments for Parkinson’s, there is extensive research on transplantation of embryonic stem cells to encourage neurogenesis, or growth of new neurons. W.C. Low (1982) showed that transplantation of embryonic dopamine neurons into the brains of animals with animal model Parkinson’s has been shown to improve many of the impaired motor functions. Lindvall and associates (1989) provide moderate evidence in support of embryonic dopamine implants improving human Parkinson’s patients motor functioning.
There is much work that has been done but also much work to be done in the study of neurodegenerative diseases. As research progresses, many similarities appear relating these diseases to each other on a sub-cellular level. These similarities offer hope for therapeutic advances in not just one, but many neurodegenerative diseases simultaneously.