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Linking Brain and Behavior:
Reflections on Neurodegenerative Diseases and Fetal Neural Transplantation

Meera Sangaramoorthy

Neurodegenerative diseases are caused by malfunctions within the motor sector of the nervous system. These malfunctions, which are caused by the presence or absence of hormones, are a direct result of neural cell deterioration within the brain. Thus, biological problems of the brain, or rather predicaments arising between cellular connections within the brain, and the treatment of such conditions, illustrate how the brain organizes movement and behavior (11).

The brain is the body's communication headquarters. It obtains a myriad of information from various parts of the sensory system and processes this information in an organized fashion. It then relays sensory input to different parts of the motor system. Such messages from the brain dictate specific muscular and behavioral patterns. Thus, this neural system is highly depended on a cause and effect system, where the slightest offset to the assembly-line fashion of cellular interaction results in major behavioral abnormalities(11). Moreover, there are two particular areas of the brain that are specifically related to motor malfunctions: the substania nigra and the striatum (the caudate nucleus and the putamen). The cells of the nigra synapse with cells of the striatum, which serves as the controller of motor functions such as walking, balance, and muscular movement. Information from the nigra cells passes through the synapses with the aid of a specific hormone, dopamine, which is a significant chemical transmitter in the brain. Because the existence of dopamine is essential to the function of the substania nigra, it is also essential for the various muscular activities controlled by the striatum, such as walking, balance, etc (9).

Neurodegenerative diseases, like Parkinson's Disease and Huntington's disease, thus, illustrate two very different behavioral patterns that are subsequently caused by two opposite and extreme biological abnormalities, where the nigra-striatum neural communication assemblage is hampered. Parkinson's disease (PD) results from a depletion in the amount of dopamine produced by the brain. At the onset of the disease, dopamine-secreting cells of the substania nigra, either because of genetic factors or environmental toxins, experience mass cell death. Thus, the nigra cells are unable to form synapses through which they secrete and relay dopamine to the striatum in a neural circuit within the basal ganglia (11). The striatum is also a coordination center for chemical messengers. When there is a decrease in dopamine levels, the striatum experiences a chemical imbalance (2). Since the basal ganglia plays a largely inhibitory role on the spinal motor centers, the loss of control of the nigra of the striatum as well as the disabilities of the striatum due to abnormal dopamine levels cause inhibition of muscular movements (11). Therefore, as a consequence of microscopic dysfunctions, macroscopic abnormalities arise. As an example, the symptoms associated with PD, are rigidity, tremors, slowness and/or no movement, loss of balance and other physical ailments (9) which also lead to psychological conditions like depression and stress (10).

Huntington's disease, like Parkinson's, is also a condition due to cell death in the brain (basal ganglia). This disease is caused by an abnormal gene that codes for a mutant protein called huntingtin. Huntingtin interferes with normal brain cell functions by causing a depletion in neural cellular energy and neural death (7)(5).

Huntington's disease (HD) can also be described as being the opposite condition to PD, both behaviorally and biologically. Instead of being the result of a hyper-inhibitory response by the striatum, HD is caused by the death of inhibitory striatum cells. In general, a hormone, called GABA, produced in the striatum regulates the levels of dopamine in the brain through an inhibitory relationship. But in HD, because of the death of GABA-producing cells in the stratum, there is an over production of dopamine. Therefore, the inhibitory check on the motor system of the body is weakened and the symptoms of HD become apparent (11). These symptoms include random muscular movements, difficulty in motor coordination (7), dementia, and loss of many psychological functions (11).

One of the possible but currently experimental treatments for both PD and HD is fetal neural transplantation. This surgical procedure is just as complicated as the diseases themselves. The biopsy entails taking precursors of adult basal ganglia cells from fetuses (several weeks old) and putting them into the caudate nucleus and putamen (divisions of the striatum) of patients. The theory behind the transplant is to allow fetal neurons to replace lost striatum cells by forming new synapses with existing recipient cells (in order to produce neurotransmitters (4)) and by connecting themselves into the basal ganglia circuit. There is observable but gradual improvements in patients who have had transplant surgery, for the fetal cells need time to grow, differentiate and make novel connections with surrounding host neurons, especially dopamine-receiving cells (6). Thus, taking dopamine-producing tissues of fetuses, putting them in a liquid suspension, and implanting them into the striatum (damaged parts of putamen and/or caudate nucleus) of a HD or PD patient has proved to be a promising surgical technique for the alleviation of neurodegenerative diseases (1)(8)(3).

Reflecting on all the observations above, it is pertinent that a general theory be formed about the structure and intricacies of the brain. Indeed, chemical and cellular malfunctions within the brain result in direct behavioral consequences. But what does this tell us about the structure of the brain itself and the relationship between the central and peripheral nervous system? The general conclusion here is that there must be a physical link, between neurons in the brain and from the brain to other parts of the nervous system, that is crucial to behavioral patterns. One can also see how the illustration of the brain as being a "box" composed of several inter-linking, smaller boxes, is apparent. For example, in PD, when the substania nigra "box" fails to achieve direct contact through axon connections with the striatum "box," the output from the striatum is severely effected. There is no other sector of the brain that could over power the malfunction of the nigra cells by "telling" the cells of the striatum what the problem is. Nor does another part of the brain stimulate cell differentiation in order to produce more dopamine. Therefore, the exiting neural impulses from the striatum "box" tend to have abnormally high dopamine transmitters (HD) or abnormally low transmitters (PD). Thus, the pattern of motor neural potentials that arrive at a muscle is also atypical. Moreover, the actions of such muscle groups in PD and HD, apparent through the myriad of physical and psychological symptoms that they depict, support this line of reasoning (11).


Web Articles

1. A Comparison of Neurosurgical Procedures

2. American Academy of Neurobiology

3. Early Postoperative Results in Ten Huntington's Disease Patients.

4. Fetal Nerve Cell Transplantation.

5. Huntington's Disease

6. Neural Transplantation for Huntington's Disease

7. Neurosurgical Horizons in the Treatment of Huntington's Disease

8. Neurotransplantation Latest Stab at Incurable Brain Disease

9. What is Parkinson's?

10. Young Parkinson's Handbook


11. Delcomyn, Fred. 1998. Foundations of Neurobiology. New York: W.H. Freeman and Company, pg. 436-437.

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