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Future Directions of Alzheimer’s Disease

May 19, 2014

Genetics, Brain Structure, and Behavior: Future Directions Alzheimer’s disease

Alzheimer’s disease is a progressive degenerative brain disease which causes the loss of cognitive functioning and behavior abilities (U. S. Department of Health and Human Services, 2014).  This disease is known for its destruction of memory (U. S. Department of Health and Human Services, 2014).  Most people are found to start showing signs of Alzheimer’s around age sixty (U. S. Department of Health and Human Services, 2014).  The exact cause is unknown, but researchers continue a diligent search for answers (U. S. Department of Health and Human Services, 2014).

Behavior Changes

Normal tasks such as paying bills become burdensome as concentrating becomes more difficult causing tasks to take longer to complete (U. S. Department of Health and Human Services, 2014).  The slow loss of memory begins to make regular daily tasks such as driving difficult as memory recollection becomes harder (U. S. Department of Health and Human Services, 2014).  A person may take a simple trip to the local grocery store and become lost and forget why or how they got there because confusion sets in (U. S. Department of Health and Human Services, 2014).  Understanding things happening at a different point in time is difficult as memory is slowly stolen from them (U. S. Department of Health and Human Services, 2014).  Communication becomes difficult because they may forget what they were speaking about so they may substitute a word that makes no sense (U. S. Department of Health and Human Services, 2014).   Judgment becomes poor and difficult which may lead to false accusations or outbursts due to frustration over something misplaced (U. S. Department of Health and Human Services, 2014).  Personal hygiene and grooming become neglected along with paying bills and hobbies (U. S. Department of Health and Human Services, 2014).  Feelings of suspicion, depression, anxiety and fear take over as their memory disintegrates and brings on confusion (U. S. Department of Health and Human Services, 2014).    At any time, a sudden outburst may occur if feelings of discomfort arise because they have forgotten they are sitting in their own home (U. S. Department of Health and Human Services, 2014).

Changes in the Brain

Studying the brains of Alzheimer’s patients has brought to light four primary neurological changes (National, 2014).    Amyloid plaques are clumps of beta-amyloid peptides combined with bits and pieces of proteins, neurons and nerve cells that have formed into a plaque that blocks the signaling between cells and synapses (National, 2014).  In a healthy brain, these things are naturally discarded, but researchers do not know what causes them to stick around in an Alzheimer brain (National, 2014).  Neurofibrillary tangles, or NFT’s, are the abnormal collection of the protein tau, essential for cell structure and shape (National, 2014).  Tau twists and clumps together inside the neuron which interrupts the cell function and causes the neuron to die (National, 2014).  The amyloid plaques and NFT’s are believed to block the synapses of neurons, breaking their connections which are essential to maintain proper function, thus bringing the neurons to their death (National, 2014).  When neurons die, it causes that area of the brain to atrophy and tissues shrink, resulting in a smaller than normal brain (National, 2014).  As the areas of the brain slowly atrophy, changes in behavior and function, begin to surface (National, 2014).  Increases in progression cause more neurons to die and brain tissue to shrink, eventually resulting in the death of the person (U. S. Department of Health and Human Services, 2014).

Potential Diagnosis Problems

Diagnosing Alzheimer’s has proven a difficult task for doctors since there are several types of dementia, all of which portray similar symptoms, however, there is not one symptom specific to Alzheimer’s (Chapman, 2005).  Presently, diagnosing is achieved through clinical testing of cognitive ability combined with neuropsychological tests, however, this is not a truly reliable diagnosis since there are no specific surface symptoms to Alzheimer’s (Craig-Schapiro, Fagan, & Holtzman, 2009).  A definitive diagnosis of Alzheimer’s disease requires a pathophysiological evaluation obtained in an autopsy (Craig-Schapiro, Fagan, & Holtzman, 2009).

A study using event related potential (ERP) brain measures in which the use of an electroencephalogram in combination with letter and number cognition tests, in collaboration with a control group of non-alzheimer’s participants versus clinically diagnosed participants of like age comparisons (Chapman, 2005).  Through the testing, researchers hoped to find a way to pinpoint what part of the brain the neurological degeneration originates (Chapman, 2005). Using more varied testing of information processing combined with a more formal measurement method (EEG), results will yield more positively towards a specific area of evolution of the disease (Chapman, 2005).  The results showed there were more amplitudes produced by the Alzheimer’s participants than were the control, however, where the degeneration begins has not been established (Chapman, 2005).

Researchers also proposed a study in an effort to identify the biomarkers of Alzheimer’s (Craig-Schapiro, R., Fagan, A. M., & Holtzman, D. M., 2009).  The effort of this study  is to be able to diagnose the neuropathology of Alzheimer’s disease before the clinical symptoms display themselves in addition to the possibility of predicting the progression of the disease and treatment response (Craig-Schapiro, R., Fagan, A. M., & Holtzman, D. M., 2009).   The plan is to use fluid and imagery markers in order to identify NFT’s and plaques at an early stage before they cause dementia (Craig-Schapiro, R., Fagan, A. M., & Holtzman, D. M., 2009).   Fluid testing should consist cerebral spinal fluid, plasma, and urine for increased tau and amyloid (Craig-Schapiro, R., Fagan, A. M., & Holtzman, D. M., 2009).   The use of imaging tests include MRI’s and PET scans of all variations to identify the plaques and NFT’s before they block communication between cells (Craig-Schapiro, R., Fagan, A. M., & Holtzman, D. M., 2009).   Being able to find these abnormalities will increase the chance of positive results from treatment and implementing early intervention measures (Craig-Schapiro, R., Fagan, A. M., & Holtzman, D. M., 2009).

Current Prevention Measures

Neurologist Robert Friedland claims the brain ages by the way and amount it is used (Marx, 2005).  Friedland implies that regular exercises and consistent brain stimulation will help slow the degenerative disease (Marx, 2005).  Research shows that people with higher education levels do not develop alzheimer’s dementia until later than the average Alzheimer patient because education has given the person a larger cognitive reserve postponing dementia (Marx, 2005).  The speculation that exercise slows degeneration is not a heavily relied upon theory because studies reveal mixed results leaving to  much variation in results to make the hypothesis true (Marx, 2005).  Researchers have also found that it may be possible that the lack of education and brain stimulation, as well as lack of physical motivation, may be pre-warning signs of Alzheimer’s disease since those who lack motivation and education develop and progress faster than those with little to no motivation (Marx, 2005). Additional research found that genetics plays a vital role in the development of Alzheimer’s disease (Marx, 2005).    These are just a few ideas, however, there are no positively proven determent’s of Alzheimer’s disease (Marx, 2005).  Other treatments consist of drug therapies that aim to reduce the neurological degeneration occurring as well as the behavioral aspects of the disease (Marx, 2005).  The future may hold promise to the treatment and possible cure of the disease as researchers continually stumble upon new leads and develop new ideas.

Future Therapies

The future holds promise as scientists have found that the administration of anti-amyloid antibody may slow the progress of the disease by decreasing the rate by which the plaques build up into clumps of blockage (Khan).  The use of immunotherapy is another hopeful treatment that will decrease the accumulation of plaques and slow cognitive dysfunction (Khan).  This treatment has been tested and ordered to stop due to the occurrence of meningoencephalitis in animals (Khan).  Further studies revealed that the immunotherapy activated the t-cells, so if they deactivate the t-cells, the therapy will break up the forming plaques in the brain (Khan).  A treatment used in dementia, cholinesterase inhibitors, are being evaluated to assist in inhibiting the breakdown of cell communication which will slow the progression of the cognitive effects, such as memory loss in the brain.

The Unknown

 

Alzheimer’s is a disease full of unknowns.  It is not known exactly why a person develops the disease, however, genetics does play a role in its development (Chapman, 2005).  It is not known where the disease originates in the brain, only the areas affected by the disease (Chapman, 2005).  The time in which onset occurs is unknown because the disease cannot be detected until certain behaviors surface (Chapman, 2005).  Though the brain shrinkage is believed to be caused by neuronal death, it is not proven (Craig-Schapiro, 2009).  The reason amyloid peptides form clumps in the neurons and NFT’s develop is also unknown, but these seem to be the main cause of the blockages that cause neuronal death (National Institute of Neurological Disorders and Stroke, 2014).  Finally, a cure has yet to be found, however, the future holds promising theories and treatments for sufferers.

 

References:

Chapman, R. M., Nowlis, G. H., & McCrary, J. (2005, February, 2007). Brain event-related         potentials: Diagnosing early-stage Alzheimer’s disease. Neurobiology of Aging, 28(2), 194-201. doi:http://dx.doi.org/10.1016/j.neurobiolaging.2005.12.008

 

Craig-Schapiro, R., Fagan, A. M., & Holtzman, D. M. (2009, August). Biomarkers of Alzheimer’s disease. Neurobiology of Disease, 35(2), 128-140. doi:http://dx.doi.org/10.1016/j.nbd.2008.10.003

 

Khan, A. (). The amyloid hypothesis and therapeutic targets for Alzheimer’s disease. The Journal   of Quality Research in Dementia, 4. Retrieved from http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=382&pageNumber=6

 

Marx, J. (2005). Preventing alzheimer’s: A lifelong commitment? Science, 309(5736), 864-6. Retrieved from http://search.proquest.com/docview/213614898?accountid=458

 

National Institute of Neurological Disorders and Stroke. (n.d.). NINDS Alzheimer’s Disease Information Page. Retrieved May 09, 2014, from http://www.ninds.nih.gov/disorders/alzheimersdisease/alzheimersdisease.htm

 

Team B. (2014). Lost in their Own World. Retrieved from Team B, psy/340 website.

 

U. S. Department of Health and Human Services, N. Institute o. A. (2014). Alzheimer’s Disease Education and Referral Center. Retrieved from http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet

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