Investigate the neurocognitive disorders associated with dementia (e.g. Alzheimer’s; Frontotemporal; and Lewy Body). How are they similar to one another and how are they different? What role does a counselor have in assisting clients (and their families) who are diagnosed with such disorders?

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DQ#1 Neurocognitive Disorders

  • Investigate the neurocognitive disorders associated with dementia (e.g. Alzheimer’s; Frontotemporal; and Lewy Body). How are they similar to one another and how are they different? What role does a counselor have in assisting clients (and their families) who are diagnosed with such disorders?
  • Select one of the neurocognitive disorders from the DSM-5. Investigate the differences within the disorder in deciding whether or not to provide a Mild versus Major Neurocognitive Disorder diagnosis (per the DSM-5). How would the severity of the disorder impact your work with a client?
  • Research contemporary treatments and advancements in diagnosis/assessment with traumatic brain injuries (TBI), and report back to the class at least two different evidence-based therapies that counselors can provide when treating TBI.

DQ#2 Paraphilic Disorder

  • Select one paraphilic disorder, and describe in detail the DSM-5 characteristics/criteria of that disorder as well as treatment recommendations. How might your treatment recommendations be impacting by a client’s age, cultural background, or other ethical factors?
  • As a future counseling professional, would you consider working with a client who has been charged with pedophilia? For example, how might your personal values, beliefs, culture or religion influence your decision? Please be sure to support your response with scholarly sources.






Alzheimer’s Disease b y B ra n d o n J. P e te …a thief o f the m in d …” 72 | AM T Events June 2016 Alzheimer’s, also known as “a peculiar disease,” has been a thief of the mind for over a century now. It is still unknown how many families deal with loved ones who lose mem­ ory of their life’s greatest times. It is something that isn’t talked about enough due to being a non-physical disorder. This is backed up by the fact that the Alzheimer’s Association wasn’t founded until 74 years after its known discovery. There is more funding and research going on now than ever before. I have become encouraged for the future of treat­ ment after diving into this research head first. Of course, we must begin all investigation with the history of its matter. The year was 1906 when German doctor Alois Alzheimer ignited the fire of this disease by a simple clini­ cal relationship with his patient. Alois saw she had the same symp­ toms which we see in Alzheimer’s patients today. He found that her brain had great shrinkage and depos­ its around damaged nerve cells. He was celebrated as a role model for taking the initiative to examine neurodegenerative disorders. In 1910, Emil Kraeplin coined the disease name after colleague Alzheimer in the eighth edition of Iris book enti­ tled “Psychiatrie.” By popular sup­ port, it would forever be known as Alzheimer’s disease. Two decades passed before the next major milestone for studying the brain occurred. Max Knoll and Ernst Ruska co-invented the elec­ tron microscope, which allowed for objects to be magnified by one mil­ lion times. There was a slight delay in mainstream research settings using the instrument until after World War II was over. Then, in the controversial year of 1968, research­ ers developed the first validated measurement scale for testing cogni­ tive and functional decline in older adults. It was an attempt to correlate the degree of measured impairment with estimates of the number of brain lesions and the volume of dam­ aged tissue. As the 70s decade drew near, the modem research era for aging disorders like Alzheimer’s came into fruition. A huge success in the fight against the disease was Congress passing the act which established the National Institute on Aging as one of our National Institutes of Health in 1974. Going forward, it became the primary federal agency backing extensive Alzheimer’s research. In 1976, neurologist Robert Katzman published an editorial in Archives of Neurology where he identified Alzheimer’s to be the most common cause of dementia and a major pub­ lic health issue. In 1979, Jerome Stone and other family support group reps had a meeting with the National Institute on Aging. They expressed the need for a national, private, nonprofit organization to coincide and stimulate federal efforts on Alzheimer’s disease. In 1980, that discussion provided the foundation to form the Alzheimer’s Association, with Jerome Stone being president. There has been over three hundred mil­ lion dollars awarded to 2,100 different research projects since 1982. In 1983, Congress designated November as the first Alzheimer’s Disease Month. The next year, the National Institute on Aging started funding a network infrastructure of Alzheimer’s disease centers at flagship medical institutions nationwide. The year 1987 brought on the first Alzheimer’s drug trial using the drug Tacrine that specifically targeted symptoms of Alzheimer’s dis­ ease. It also gave birth to the identifying of the first gene associated with uncommon, inherited forms of Alzheimer’s disease. Along with identifying Beta-amyloid protein and Tau protein, came the emergence of treat­ ments. The 1990s brought great awareness and momentum as the disease popular­ ized. hi 1993, the APOE-e4 gene on chro­ mosome 19 was the first risk factor gene discovered. That same year, Tacrine (Cognex) was approved by the FDA. In 1994, President Reagan announced his being diagnosed with the disease and the Alzheimer’s Disease International made September 21st World Alzheimer’s Day. Before the turn of the century, the first Alzheimer’s vaccine was proved to be successful in mice. Scientists injected them with beta-amyloid proteins that stopped developing plaques and other similar changes to the brain. The new millennium was believed to show much progress and hope in the Alzheimer’s community. In 2003, The Alzheimer’s Association and National Institute on Aging led a national Alzheimer’s disease genetic study. This was a federal initiative to collect and bank blood samples from families with several members who developed Alzheimer’s in their later years to find more risk genes. The first report on the Pittsburgh Compound B (PIB) was shared at the Alzheimer’s Association International Conference on Alzheimer’s disease (AAICAD) in 2004. It proved to be a potential breakthrough by allowing the positron-emission tomog­ raphy to enter the bloodstream and attach itself to beta-amyloid deposits for detection. During the same year, the Alzheimer’s Association began to sponsor the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Its ultimate goal is to determine whether standardized imag­ es can identify high-risk individuals; provide early detec­ tion; and track and monitor treatment effects in clinical trials of disease-modifying drugs. During the second half of the decade, the Alzheimer’s Association launched the journal A lzheim er’s & Dementia. In 2008, The International Society to Advance Alzheimer Research and Treatment formed as the first and only professional society specifically for Alzheimer’s and dementia. With the need for global information trans­ mission, the Alzheimer’s Association International Conference on Alzheimer’s disease became annual in 2009. With everything set in motion, the present decade kicked off with setting a national agenda. This was appar­ ently important, with the CDC releasing statistics show­ ing that Alzheimer’s had climbed to the number six lead­ ing cause of death. In 2011, President Obama signed the National Alzheimer’s Project Act (NAPA) into law. It was consid­ ered to be groundbreaking as the first national strategic plan to address the crisis and to attune the research, care, and support fronts. The association created the Alzheimer’s Breakthrough Ride to unite funding and awareness for effective treat­ ments among researchers. A clinical tri­ als database was formed by the associa­ tion and Coalition Against Major Diseases who allowed qualified researchers to have easy access. The association also created the Trial Match tool for Alzheimer participants to choose clinical studies that might be a good match. This is accepted as a great strategy to have expe­ dient treatment development. W arning Signs of A lzh e im e r’s The most commonly known symptom is a lack of ability to obtain newly acquired information due to brain damage in the part of the brain affecting learning. Later symptoms include disorientation, confu­ sion about events, unfounded suspicions about family, and difficulty speaking, swallowing, and walking. There are ten major warning signs. Patients may have a com­ bination of signs that affect them on different levels. Each one should be taken seriously and discussed with a physician. Number one is memory loss that disrupts daily life, and repeatedly asking for the same information. They have challenges in planning or solving problems and working with numbers. People show difficulty completing famil­ iar tasks like remembering the rules of a favorite game. They may have confusion with time or place like forget­ ting where they are or how they got there. Some experi­ ence trouble understanding visual images and spatial relationships. A patient may have new problems with words in speaking or writing. Others struggle with mis­ placing things and having issues retracing back. They display poor judgement and awareness of themselves and others. A slight withdrawal from hobbies, work, and (continued on page 74J AMT Events June 2016 73 ALZHEIMER’S DISEASE (continued fro m page 73) social activities might occur. Lastly, changes in mood and personality take place when certain routines switch. The next question to answer is how individuals with Alzheimer’s function daily. As you can expect, the day-to-day functioning of a per­ son with Alzheimer’s disease can affect their lifestyles in numerous ways. It can progress into an unstable sleeping pattern for the patient. They will usually not be able to sleep properly for long periods of time. It may seem as if their days and nights are all jumbled up. Waking up in the middle of the night and wandering around the house isn’t uncommon either. Whoever watches over them normally makes sure that they use the restroom before bed as well. Patients also end up having a lack of self-awareness and care, such as bathing regularly. Patients sometimes forget about keeping up their hygiene normally. This is due to fears of water or lack of privacy for the most part. With memory loss, simple func­ tions like working a faucet and taking a bath seem very complex to them. Caregivers are very distinctive, sequen­ tial, and firm when directing them on bathing. Patients are encouraged to dress themselves until it becomes too difficult a task. Once patients wake up or get out of the bathtub or shower, caregivers must take certain mea­ sures to prevent frustration. Some people lay out their patient clothes in the order of use. Also, caregivers must remember to never ever rush the person suffering with Alzheimer’s. After preparation, their mealtimes can easily be the highlight of the day. They range from overeating to eating inadequate amounts due to sense of taste and smell loss. Caregivers must make sure that the mealtime routines are constant from day to day. Cutting their food into pieces and giving them small utensils assist in preventing overeating. If they are eating, it also means going to the bathroom shall follow sometime after. Something simple as getting to the bathroom in time can really affect an Alzheimer’s patient. They could forget where the bathroom is and struggle with expressing their needs to go. Most of the time they will give non-verbal cues to show something is wrong. As the disease worsens, it becomes more appar­ ent that they need to start wearing adult diapers. My grandmother Hazel has been going through the onset of Alzheimer’s for the past two years now. It really has been a shocking experience as it unfolds under my eyes. The first time I heard anything strange about her behavior was during winter break of 2012.1 did not make it to Louisiana until Christmas day due to work that year. 74 A M T Events June 2016 On my arrival, I was pulled to the backroom by my uncle who had a disturbed look on his face. He told me that my grandmother went to sleep with food cooking on the stove Christmas Eve night. If it wasn’t for him waking up, who knows what could have happened. I asked my grandmother, but she had no recollection of cooking. The next incident that happened last year had to do with my cousin this time. My dad, uncles, and aunts con­ vinced him to move in with my grandmother at the begin­ ning of summer 2013. He told me one day she woke up from hearing some noise in the kitchen. It was my cousin cooking and she seemed startled while opening her room door. She asked, “Who are you?” in the most genuine voice as possible. Of course, my cousin didn’t think any­ thing of it at first. So once again she asked the same question in a louder tone and he answered, “It’s me, Odin, maw-maw.” My grandmother went back to her room and dialed my Aunt Connie’s phone number. She asked where she was and why did Connie leave her in a stranger’s house. That was just strike two in my book. The final straw happened this past summer for the same incidents. She experienced two hospital visits for passing out and having a TLA mini stroke within three months. My grandmother does not like drinking water and becomes very dehydrated at times. I thought it had to do with her taste buds changing at first. After running tests, the doctor told us she had a urinary infection both times. I figured she was dealing with a nosocomial infec­ tion but something told me to further investigate. I saw some websites and articles linking Alzheimer’s disease to urinary infection ironically. These different incidents have made my family become concerned about her. She is a fairly healthy 85-year-old woman and I would hate for Alzheimer’s to rob her of memory. It has become urgent for me that I try talking to her every day on the phone about anything. She has so much knowledge and experi­ ence to share amongst us all. Hazel is my last living grandparent and I want to make sure she understands how much I love her while memory allows. ■ R e fe re n c e s Alzheimer’s Disease Symptoms & Stages. (2014, April 15). Retrieved November 24, 2014, from sy mptomsandstages .html Hazel Pete Personal Interview (2014, November 25). Major Milestones in Alzheimer’s and Brain Research. Retrieved November 24, 2014, from alzheimers.asp At the time of writing this article, Brandon J. Pete was a graduating senior at Sam Houston State University in Huntsville, TX, majoring in Health. Copyright of AMT Events is the property of American Medical Technologists and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder’s express written permission. However, users may print, download, or email articles for individual use. Hindawi Publishing Corporation BioMed Research International Volume 2016, Article ID 2589276, 17 pages Review Article Therapies for Prevention and Treatment of Alzheimer’s Disease J. Mendiola-Precoma, L. C. Berumen, K. Padilla, and G. Garcia-Alcocer Laboratorio de Investigación Genética, Facultad de Quı́mica, Universidad Autónoma de Querétaro, Cerro de las Campanas S/N, Centro Universitario, 76010 Santiago de Querétaro, QRO, Mexico Correspondence should be addressed to G. Garcia-Alcocer; Received 23 March 2016; Revised 31 May 2016; Accepted 5 June 2016 Academic Editor: Yiying Zhang Copyright © 2016 J. Mendiola-Precoma et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Alzheimer’s disease (AD) is the most common cause of dementia associated with a progressive neurodegenerative disorder, with a prevalence of 44 million people throughout the world in 2015, and this figure is estimated to double by 2050. This disease is characterized by blood-brain barrier disruption, oxidative stress, mitochondrial impairment, neuroinflammation, and hypometabolism; it is related to amyloid-𝛽 peptide accumulation and tau hyperphosphorylation as well as a decrease in acetylcholine levels and a reduction of cerebral blood flow. Obesity is a major risk factor for AD, because it induces adipokine dysregulation, which consists of the release of the proinflammatory adipokines and decreased anti-inflammatory adipokines, among other processes. The pharmacological treatments for AD can be divided into two categories: symptomatic treatments such as acetylcholinesterase inhibitors and Nmethyl-D-aspartate (NMDA) receptor antagonists and etiology-based treatments such as secretase inhibitors, amyloid binders, and tau therapies. Strategies for prevention of AD through nonpharmacological treatments are associated with lifestyle interventions such as exercise, mental challenges, and socialization as well as caloric restriction and a healthy diet. AD is an important health issue on which all people should be informed so that prevention strategies that minimize the risk of its development may be implemented. 1. Introduction 2. Pathogenesis and Clinical Features in AD Alzheimer’s disease (AD) is an age-related, progressive, and irreversible neurodegenerative disorder characterized by cognitive and memory impairment, and it is the most common cause of dementia in older adults. The estimated prevalence of this disease in 2015 was 44 million people throughout the world and it is estimated that this figure will double by 2050 [1]. Most people with AD (over 95%) have sporadic or late-onset AD (LOAD), a multifactorial disease in which environmental factors and genetic predisposition contribute to the pathology [2]. The other form of AD, familial or earlyonset AD (EOAD), corresponds to less than 5% of the AD population and is due to mutations in any of the three following genes: (a) the amyloid precursor protein (APP) gene on chromosome 21, (b) presenilin 1 (PSEN-1) gene on chromosome 14, and (c) presenilin 2 (PSEN-2) gene on chromosome 1 [3–5]. The classification of AD is based on clinical criteria including medical history, physical examination, laboratory tests, neuroimaging, and neuropsychological evaluation [6]. The neuropathological features of both forms of AD are characterized by the abnormal extracellular accumulation of amyloid-𝛽 peptide (A𝛽) in amyloid plaques and tau protein aggregated in intracellular neurofibrillary tangles (NFTs). There are epidemiological, clinical, and experimental data that sustain several hypotheses of AD pathogenesis: (1) the amyloid cascade hypothesis proposes that the accumulation of A𝛽 as neuritic plaques, diffuse plaques, or oligomeric forms in the brain is the main pathogenic event [7]; A𝛽 plaques are composed primarily of A𝛽 peptides generated by the amyloidogenic pathway [1]. The amyloidogenic pathway produces amyloid peptides of 39–43 amino acids that are proteolytically derived from the sequential enzymatic action of 𝛽- and 𝛾-secretases on amyloid precursor protein (APP) distributed in the neuron membrane [8, 9] while the nonamyloidogenic pathway produces nontoxic 𝛼APP fragments that are generated by 𝛼-secretase action [5]; (2) the tau hypothesis suggests hyperphosphorylation of tau as the primary event [10]; (3) 2 BioMed Research International 𝜀 oE Ap 4 o Ap E E o Ap o Ap E L LD o Ap E o Ap ABCA1 R LX E Microglia Cholesterol Astrocyte ROS ROS Proinflammatory cytokines ROS ROS pt id e A𝛽 ApoE e A𝛽 id pt Cholinergic hypothesis AChE id pt e ApoE pe Nonamyloidogenic pathway P3 PEN-1 Nicastrin APH-1 ↓ ACh ↓ ACh ACh Amyloid hypothesis ACh ACh A𝛽 plaque APP Choline 𝛽-sec Tau P P Tau Tau P pt pt A𝛽 Tau Tau P Tau id pt e pe pe Tau aggregation ↑ GSK-3𝛽 pe id A𝛽 Tau Tau e id A𝛽 ApoE P id e pe pt A𝛽 e ApoE pt ApoE ApoE ApoE pe A𝛽 LDL id e id ApoE ApoE e id pt pe ApoE ApoE pt pe e id e id pt pt e ApoE ↑ A𝛽 peptide pe pe A𝛽 LDL e id A𝛽 A𝛽 ApoE pt pe A𝛽 ↑ ROS e id NMDA HSPG-1 Ca2+ o Ap Mitochondrial hypothesis E Tau hypothesis A𝛽 peptide oE Ap Ca2+ LRP-1 pt Ca2+ Ca2+ Ca2+ LDL A𝛽 Ca2+ Ca2+ A𝛽 e id A𝛽 oligomer pe pt A𝛽 A𝛽 LDLR pe A𝛽 A𝛽 peptide APH-1 ROS ApoE A𝛽 PEN-1 Nicastrin P Tau hyperphosphorylation in microtubules PEN-2 𝛾-secretase P Amyloidogenic pathway ROS ROS Choline Choline Mitochondrial dysfunction Excitotoxicity Neuron ↓ ChAT ACh 𝛼-sec Tau Neuron i pt Choline Choline Acetate pe pe A𝛽 PEN-2 𝛾-secretase pe LDL de ApoE A𝛽 ApoE L LD oE Ap o Ap E TNF-𝛼 IL-6 ROS Oxidation A𝛽 A𝛽 A𝛽 plaque A𝛽 BBB A𝛽 oligomer Vascular hypothesis Cholesterol IL-6 TNF-𝛼 Oxysterol TNF-𝛼 Metabolic …
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