Effects of Neurochemical Production on Alzheimer's Disease

The Effects of Neurochemical Production on Alzheimer’s Disease
Jeannette Villatoro
PYJ0919A
Dr. Trent Nguyen
July 30, 2009











The Effects of Neurochemical Production on Alzheimer’s Disease

Alzheimer’s disease is a serious affliction that affects millions of people over the age of 50. One of the onsets of Alzheimer’s disease is a chemical imbalance within the brain. Such imbalances may occur from overproduction of proteins and pose a major concern for the health and well being of the elderly. One with Alzheimer’s disease may likely develop depression because of the detrimental symptoms of their disease. Many psychologists contend that depression symptoms among patients with Alzheimer’s generally have more serious and adverse effects as the progression and cohesion of these two disorders create a harmful infusion. This author will attempt to interpret research on the issue of Alzheimer’s disease in relation to chemical imbalances, what studies have been conducted to support this theory of the cause of Alzheimer’s, and how minimizing the onset of chemical imbalances has an effect on the overall disease and depressive symptoms that can occur as well.

Neurochemical Production and Alzheimer’s Disease

Alzheimer’s disease can be described as a deterioration of the brain functioning. Loss of memory ensues along with many emotional and behavioral problems that can undoubtedly arise. This disease is most common in adults that are between the ages of 60 and 90, but this unforgiving disease has shown signs of progression in even younger seniors (ADEAR, 2009). According to ADEAR (Alzheimer’s Education and Referral Center), “damage to the brain begins as many as 10 to 20 years before any problems are evident” (ADEAR, 2009, p.1). Cognition is affected in the patient with less coherent ability in memory, reasoning, communicating, and understanding. When cognitive abilities do return to the patient even mildly, depression may become induced because of the recognition of the loss of cognition (ADEAR, 2009).
The cause of Alzheimer’s disease has been long pursued and not yet discovered in its entirety. ADEAR states that “scientists don’t yet fully understand what causes Alzheimer’s disease, but it is clear that it develops because of a complex series of events that take place in the brain over a long period of time” (ADEAR, 2009, p. 1). Research that shows certain build up of proteins can possibly be the foremost contributing cause of the onset of Alzheimer’s disease and it is to date the most promising explanation of the disease. Abnormal neurochemical production in the brain and build up of proteins such as beta-amyloid are connected to Alzheimer’s disease and may be the closest clues to finding the reasoning for the inception of Alzheimer’s (Bailer, Liu, Smith, Isaacson, 2000). It is not yet apparent the deliberate cause of Alzheimer’s but chemical imbalances and brain abnormalities that are connected to the disease are plentiful. Some studies have suggested that the mutation of the APP gene produce familial Alzheimer’s disease (Carlson, 2005). Carlson surmises that certain mutations of presenilin genes also cause “the defective long form of beta-amyloid to be produced” (Carlson, 2005, p. 453) which can be a definite precursor to the disease. Along with the tangles that can occur in the brain “in an area called the entorhinal cortex, plaques form in other areas causing the neurons to work less efficiently” (ADEAR, 2009, p.1).

In one study on biometrics, it was concluded by Bailer et al. that “nerve growth factor (NGF) is a target-derived protein that promotes the survival of the same nerve cells in the mature nervous system that atrophy in neurodegenerative disorders such as Alzheimer’s disease” (cited from Bailer et al., 2000, p. 936). According to Bailer et al., the exact action of this chemical is yet unclear but it is believed to play a key role “in the synthesis and neurochemicals and cytoskeletal proteins” (cited from Bailer et al., 2000, p. 936). NGF promotes survival among the neurons that lose functioning and deteriorate when Alzheimer’s becomes evident and because of this, the same chemical is used in treating the disorder and to repair the damaged cells and salvage the dying nerves (Bailer et al., 2000).

This study focused on the biochemical measurement of neurochemical production in the brain. Because the neurochemical production and the morphological assessment of the number of axons cannot be done on the same organism, the independent measurements of neurotransmitter activity and axon production were made separately in each of the experimental groups (Bailer et al., 2000). In a particular study on NFG and its effects on such diseases as Alzheimer’s, adult rats were given NFG through a time-released pumping apparatus through intracranial infusion. The results were quite astounding in that not only did the rats show an increase in production of the neurotransmitter norepinephrine, but also had an increase in the number of axons. The study then compared the normal average neurochemical production per axon with the various experimental groups consisting of those affects with neurodegenerative disorders like Alzheimer’s and those who were adherently healthy (Bailer et al., 2000). The proven results of this study as outlined is a major improvement on the production, repair, and distribution of neural activity within the brain that particularly causes such diseases as Alzheimer’s to alleviate normal functioning in the elderly. This supports the conception that norepinphrine plays a significant role in retroactive allocation of proper nerve health. The closer these studies come to narrowing down the intricate workings of the neurotransmitters and various chemicals, the sooner a cause for Alzheimer’s as well as a subsequent cure can be found.

The chemical breakdown of proteins is a significant process within the brain. Particularly with Alzheimer’s disease, there is evidence that protein build up defies the axons to fire properly and helps aid in degeneration in Alzheimer’s patients. The Alzheimer’s Association concurs that plaques are “abnormal clusters of protein fragments that build up between nerve cells” (Alzheimer’s Association, 2009. p. 1). One study clearly focused on the similarities of Alzheimer’s patients and the amount of tangles and protein or plaque build up that was accumulated. This triggered research to determine what impact this has on the symptoms of the disease. In this study, most patients showed developed abnormalities within the brain structure and synapses transmissions. This is a huge development in the discovery of a potential treatment for Alzheimer’s in that a major percentage of patients suffer from the same chemical imbalances within the brain. It was evident in this study of 306 subjects that 258 had abnormal forms of beta-amyloid proteins and tau proteins (Bailer et al., 2000). Excessive amounts of beta-amyloid protein are thought to be responsible for the disease. Therefore, steps in prevention must focus on the same deformities within the brain that produces these toxic amounts of protein build-up.

Plaque build-up promotes nerve cells to decay and die. As noted by the Alzheimer’s Association, “dead or dying nerve cells contain tangles, which are made up of twisted strands of another protein” (Alzheimer’s Association, 2009, p. 1). In one particular study, the tangles within the interhinal cortex also showed major effect on the development of Alzheimer’s. It was concluded that several of the subjects studied in the experiment showed entanglements in addition to plaque build-up. The tangles caused abnormal neurochemical production and overproduction of serotonine in the brains of patients (Bailer et al., 2000) and the number of axons and transmissions within the neural cavity were greatly inhibited. Widespread cell death will indubitably shrink the brain considerably and also damage tissue. Consequently, most of the cortex will be damaged and advanced Alzheimer’s disease will ensue. This will mean irreparable injury to the patient’s brain functioning and severely reduced cognitive abilities. In a study of 101 males with Alzheimer’s between the ages of 56 and 72 years of age, brain PH was shown to have significant decrease compared to young male adults between the ages of 22 and 36. It was believed that a decaying exponential was at fault for the decrease in PH balance due to the plaques and tangles in the brain (Bailer et al., 2000).

Because evidence of the abnormalities seem to be present long before the onset of Alzheimer’s disease, it is important to study those unaffected by the disease in preferably earlier ages of life span. If the excessive protein build-up shows among middle-aged people, the development of brain damage that causes Alzheimer’s can be followed and understood more properly. The point in which Alzheimer’s is officially triggered has unfortunately not yet been discovered; therefore the linkage to symptoms can be explained but not the point of ignition.

Effects of Depression on Alzheimer’s Disease

Many studies have delved into the depths of Alzheimer’s disease and what causes the devastating symptoms. ADEAR states, “common behavioral symptoms of AD include sleeplessness, agitation, wandering, anxiety, anger, and depression. Scientists are learning why these symptoms occur and are studying new treatments—drug and non-drug—to manage them. Treating behavioral symptoms often makes people with AD more comfortable and makes their care easier for caregivers” (ADEAR, 2009, p. 2).

Depression and Alzheimer’s have a major relationship. Depression is not only a side effect of Alzheimer’s; it is also a potential cause for the dementia that occurs. One study focused on the depressive disorder seen in many Alzheimer’s patients not in current circumstances, but from a lifetime perspective. Those patients that experienced long bouts of depression throughout their lives had a more powerful tendency to develop Alzheimer’s (Berger, Bodian, Hirsch, 1996).

Some studies have attempted to integrate the care giving support from families with the depressive symptoms that occur. Although depression is commonly one of the major effects of Alzheimer’s due to chemical imbalances within the brain, depression can also occur when family support is lacking. Depression can occur for many reasons and usually is a result of brain abnormalities as well as environmental issues. Because the causal effects of Alzheimer’s are difficult to understand, we can determine some environmental causes from research. As Berger et al. explains, data from these studies “are obtained by first finding a group of affected person, that is, persons having or having had the disease; such persons are customarily called probands. Their families are said to be ascertained.” (Berger et al., p. 831). One study in particular focused on the particulars of family roles with Alzheimer’s patients. The study in question pertained in this article emphasizes the findings of family participation in Alzheimer’s disease and the consequences of lack of support.

The effects on the families are just as significant as the effects on the patients. Because family support is relevant to the patient’s well being and how they cope with the disease, it is important to study the family in relevance to the onset of Alzheimer’s. Berger et al. shows that that this particular research also highlighted the “age-specific and lifetime risks of a late on-set disease when families are ascertained through probands” (Berger et al., 1996, p. 833). Family support is imperative for Alzheimer’s disease to be handled, and most patients unfortunately lack this support. Most family members do not know how to handle the onset of Alzheimer’s and tend to leave the patient in the hands of care giving facilities. In a study of more than 130 Alzheimer’s patients and their respective families, persons from about 83 families out of the 132 studied admitted to either losing interest in the care of the Alzheimer’s patient, being stressed about the disease, showing lack of support for the patient, or backing away due to a deficiency in knowledge or understanding of the disease. Those people from 68 out of those 83 families said that they would more likely be a significant support in the life of the Alzheimer’s patient if ongoing counseling and support was given to the family (Berger et al., p. 833). This is a major complication in the life of a patient with Alzheimer’s, as familiarity and comfort are essential elements as the onset of the disease becomes more present. Having a deficiency in these areas of life have been proven to create a more depressed attitude within the patient and therefore enable the disease to progress more rapidly (Berger et al., 1996, p. 833). Severe Alzheimer’s disease may be sadly immanent, with depreciated cognitive ability, memory and normal brain functioning. With advanced onset of Alzheimer’s, death is a forthcoming tragedy. It is significant to deter depression from becoming a more aggressive suitor of the disease.

One of the underlying factors of lack of family support shows that depression most likely becomes evident. This is a major concern for Alzheimer’s patients due to the effect depression has on the brain. Carlson gives the information that “depression is caused by insufficient activity of monoaminergic neurons” (Carlson, 2005, p. 479). Treatment is available for depression with much success, but the difficulty in treating depression in Alzheimer’s patients is that the effects of the drugs also have negative effects on the disease and the symptoms that are caused by the disease (Carlson, 2005). The treatments that work for depression are primarily through drugs that affect monoamines such as norepinephrine and serotonin. This interferes with the neurochemical production for Alzheimer’s as well as inhibiting the drug treatments that act as an agonist for the synapses that affect the brain in Alzheimer’s patients. Because of this, it is important to prevent depression by allowing support to the patient to be strong. The chemical imbalances that cause depression are difficult to treat, but the environmental occurrences that enable depression to enrapture an Alzheimer’s patient can definitely be controlled.

Alzheimer’s disease is a fascinating form of dementia that is initiated by several brain abnormalities and chemical dysfunctions that occur within the life span of a young adult to an elderly individual. Alzheimer’s disease currently has no cure and very limited treatment possibilities, and it ultimately causes death. Many studies have been done to deliberately find the causes of Alzheimer’s disease and although the studies are not conclusive, there have been many breakthroughs in research to date. Studies have shown incredibly high percentages of Alzheimer’s disease in patients with reoccurring bouts of depressive disorder. The build-up of certain proteins along with entanglements in the interhinal cortex is proven to produce Alzheimer’s. Yet the actual igniting factors of the disease are yet to be established. Many symptoms of this disease prove to be distressing for the patient and family alike. Depression is a major symptom of Alzheimer’s along with being a possible cause for the disease. By understanding the link between depression and Alzheimer’s, and uncovering site attractions within the brain that are most affected by harmful plaque accumulation and nerve cell entanglements, scientists can indeed begin a path of discovery that can better treat and possibly prevent Alzheimer’s from occurring.

















References
ADEAR, (2009). Alzheimer's disease fact sheet. Retrieved July 30, 2009, from National
Institute on Aging Web site: http://www.nia.nih.gov/Alzheimers/Publications/adfact.htm.
Alzheimer's Association, (2009). Plaques and tangles. Retrieved August 17, 2009, from
Alzheimer's Association Web site: http://www.alz.org/brain/10.asp.
Bailer, A., Liu, S., Smith, M., Isaacson, L., (2000). Statistical comparison of axon-
scaled neurochemical production. International Biometric Society, 56, Retrieved August 1, 2009, from http://www.jstor.org/stable/2676945.
This article pertains to a study that was introduced on the neurochemical production and how the buildup of proteins can be considered a huge cause of neurodegenerative diseases such as Alzheimer’s disease. This study performed research on adult lab rats that ultimately proved that the chemical NGF helped to repair dying nerves. This study also focused on experimental groups with Alzheimer’s diseases and those without it to determine the normal neurochemical productions in relation to axons to determine the normal ration as compared to the experiment on the rats. The target population was the elderly susceptible to Alzheimer’s disease. This article was instrumental in discovering the effects of neurochemical production and how it supports treatment of damage to nerves that cause the symptoms and deterioration one faces in Alzheimer’s disease.
Berger, A., Bodian, C., Hirsch, W., (1996). On estimating incidence rates of diseases
with delayed onset using biased samples. Journal of the American Statistical association, 91, from http://www.jstor.org/stable/2291678.
This article focuses solely on the rates of incidents of Alzheimer’s using onset techniques. Specific affected groups were sampled to research effects of the disease on patients. The focus of this article was mainly the deterioration by diseases that accumulate later in life as opposed to those diseases, which are born to persons. This article also deals with research on heredity of the disease.
Carlson, N. (2005). Foundations of physiological psychology (6th edition). Boston, MA: Pearson Education.