Alzheimer's+Disease+and+Its+Diagnosis+Process

=History=

Alzheimer's Disease was discovered in 1906 by Dr. Alois Alzheimer who was treating a patient with symptoms like "profound memory loss, unfounded suspicions about her family, and other worsening psychological changes." In 1968 the cognitive scale was determined for diagnosing this unknown disease. The primary suspect in cell damage and deterioration was identified in 1984: the beta-amyloid. Drug trials for medication and prevention began in 1987 and clinical studies in 1991. The first drug for treatment, Cognex, was approved by the FDA for distribution and use in 1993. Genetics studies began in 2003 determining the presence of Alzheimer's related genes. Potential markers of the progression of the disease began in 2009 with cerebrospinal fluid. 2011 marked a new standard for diagnosis Alzheimer's disease when the guidelines were published in the National Institute of Aging. And concluded in 2014 was the fact that more deaths were related to the disease than previously reported, grabbing some attention on the matter of diagnosing.

=Symptoms=


 * Memory loss
 * Brain atrophy, a loss of size and volume due to shrinking
 * Challenges related to thinking ahead and planning
 * General confusion
 * Language issues in areas of speech or writing
 * Unable to retrace steps
 * Poor or lowered judgment
 * Mood/Personality changes
 * Withdrawing one's self from their originally normal life routines (work, family, etc)

Note that not all of these symptoms show in one individual. This disease differs from brain to brain, so any combination of these could warrant a visit to the doctor's. = = =Diagnosis Process=

Four major steps and exams are done to diagnose this disease. The patient's tells a history of recent symptoms which usually is verified by close friends and family, physical tests with blood and urine to rule out other causes, brain scans including MRI and PE T to look at brain atrophy and/or tumors, and neuropsychological evaluations which test language, memory, attention, and skills with mathematics. The results are then looked at and a conclusion is drawn.

**Healthy, Non-dementia Aging**

Aging is a natural phenomenon which affects every living organisms. The aging of a brain, then, is not an exception to the matter. "Normal" aging depends on the person and their brain, therefore affecting each person differently but relatively the same. The pre-frontal cortex is the most affected in size with aging where as the occipital lobe is the least affected. Gray and white matter loss lead to a "shrinking" brain. On average, healthy patients lose 1.32 and 2.40 cm in gray and white matter losses respectively. Other areas of the brain thin due to this loss of gray and white matter loss like the lateral frontal lobe, temporoparietal lobe, superior temporal lobe, lateral occipital lobe, and the isthmus cortex. These volume losses can affect a whole slew of things because of the brain being in control of everything. The volume loss in one area could be detrimental, but could also show now symptoms or changes. Because the brain's plasticity (ability to change connections and communication paths) is high, it can alter areas to help others work better without really affecting the initial area. Normal, healthy aging can be prevented by remaining in-shape and playing brain games to teach yourself something new and keep the brain's plasticity high.

=The Diagnosis Process in New Light=

The process of diagnosing this disease requires qualitative data and comparison scans/results to determine a conclusion. Many of these symptoms like memory loss and brain atrophy are healthy in the aging process, as mentioned above. There are other areas of the brain whose changes caused by normal aging should create no to little symptoms: hub networks and cognitive reserve. The symptoms of these changes can be quantified and can lead to a better understanding and conclusion of diagnosis.

Hub regions integrate information of the brain and relay that information to other portions of the brain. If these are interrupted or damaged, the brain's reaction time is slowed. Hub regions weaken when the power decreases which is accompanied by an initial rise of spike densities on average before a final slowing sets in. (de haan) These spike densities, which can be recorded in one fMRI session, can be computed into a prediction pattern for the disease itself as well as its progression.

Cognitive reserve is the brain's compensation for specific damage in areas. A higher cognitive reserve, which can also pull in areas that are not specific to that action causing them to wear and tear, correlates a higher measure of injury in most cases. Cognitive reserve can be quantified in one fMRI session as well using the DTI data. These two factors reviewed together can define a concluding diagnosis that previously used at least four tests, usually more than four including follow-ups, to diagnose.

= References =

“Major Milestones in Alzheimer’s and Brain Research.” // Alzheimer’s Association & Alz.org. // 2014. Web. 19 July 2016. “10 Early Signs and Symptoms of Alzheimer’s.” //Alzheimer’s Association & Alz.org.// 2016. Web. 19 July 2016. Press Office. "Largest-ever Alzheimer's gene study underway." //Sanger Institute//. 2007. Web. 19 July 2016. “Screening and Testing for Alzheimer’s Disease.” //Brightfocus.org//. 2016. Web. 19 July 2016. Resnick, S, Pham, D, Kraut, M, Zonderman, A, Davatzikos, C. "Longitudinal Magnetic Resonance Imaging Studies of Older Adults: A Shrinking Brain." //The Journal of Neuroscience// 23.8 (2003): 3295-3301. Web. 19 July 2016. De Haan, W, Mott, K, van Straaten, ECW, Scheltens, P, Stam C. "Activity Dependent Degeneration Explains Hub Vulnerability in Alzheimer’s Disease." // PLoS Computational Biology. // 8.8 (2012): 1-14. Web. 19 July 2016.

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