A Literature Review Of Alzheimers Disease Biology Essay

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Ten years ago, few Americans had ever heard of Alzheimer’s Disease. Yet, today, this progressive and irreversible brain disease is recognized as one of the most devastating maladies of our time. AD causes a steady decline in memory and is the leading cause of dementia or the loss of intellectual abilities, thinking, remembering and reasoning, which are severe enough to interfere with a person’s daily functioning at work or home. Nearly 53,000 elderly in Mississippi alone have AD. AD affects people regardless of sex, race, ethnic group or socio-economic circumstances (Living with Alzheimer’s, 2009). It is the seventh leading cause of death among American adults (Dillard, 2009). AD will be the epidemic of the 21st century. According to the Alzheimer’s Association (1998), by the time baby boomers reach the age of greatest risk, 14 million Americans will have the disease.

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In 1906 a German physician, Dr. Alois Alzheimer, specifically identified a collection of brain cell abnormalities as a disease. One of Dr. Alzheimer’s patients died after years of severe memory problems, confusion and difficulty understanding questions. Upon her death, while performing a brain autopsy, the doctor noted dense deposits surrounding the nerve cells (neuritic plaques). Inside the nerve cells he observed twisted bands of fibers (neurofibrillary tangles). Today, this degenerative brain disorder bears Dr. Alzheimer’s name, and when found during an autopsy, these plaques and tangles mean a definite diagnosis of AD (American Health Assistance Foundation, 2010). A general timeline of the progression of AD reveals that research has come a long way, but there are still hurdles to cross in the present and the future. Following is a detailed list of milestones that have been achieved regarding AD.

Alzheimer’s Historical Timeline

1906: Dr. Alois Alzheimer

Dr. Alois Alzheimer first reports the hallmark pathological changes of AD found

in the brain of patient Auguste D. in a meeting at Tubingen. He was the first to describe the fibril tangles associated with the disease.

1960s: Alzheimer’s Disease Recognized as a Disease

The discovery of the link between cognitive decline and the numbers of plaques and tangles in the brain leads medical scientists to finally recognize AD as a “disease,” not a normal part of aging.

1970s: Scientific Interest in Alzheimer’s Disease is Awakened

Scientific advances bring new tools, techniques and knowledge to the exploration and understanding of the human body. The disease emerges as an area of research interest.

1978: Alzheimer Society Founded (the first organization of its kind in the world)

The Alzheimer Society is formed to help families caring for someone with the disease and to promote research into treatments, prevention and a cure.

1980s: Research Focuses on Plaques and Tangles

Researchers examine the complex interactions that are harming nerve cells in the Alzheimer-diseased brain. Researchers focus on the chemistry of the toxic proteins identified as “amyloid” in plaques and “tau” in tangles. This research assists in the genetic breakthroughs in the 1990s.

1990s: Giant Leaps Forward

Teams of scientists discover genetic links to AD. In turn, this leads to the creation of mice models of the disease, allowing research testing that had not been possible previously.

1992: An Essential Piece of the Alzheimer Puzzle

The first real genetic link to the disease is discovered — a mutated gene in the majority of familial Alzheimer cases that influences a person’s risk of getting the disease. Although this form is rare — roughly seven per cent of the Alzheimer population — this is a crucial discovery.

1993: Major Risk Factor Identified

Once again, scientists make major advances — this time identifying the role of the apoE gene in the brain.

1997: First Drug Treatment Approved

The first drug, a “cholinesterase inhibitor” known as Ariceptâ„¢ becomes available that lessens the symptoms of mild to moderate AD in some individuals. Two new cholinesterase inhibitors, Exelonâ„¢ and Reminylâ„¢ are developed over the next five years, offering treatment alternatives.

1999: First Vaccine is Tested

The first AD vaccine is developed and tested using mouse models — a significant achievement. The work on vaccines continues to show great promise.

2000: Sophisticated Imaging of the Living Brain

Technological advances in imaging provide a new window into the living brain. Images indicate that changes may exist in the brain long before a person develops symptoms of AD.

2004: New Drug Therapy Approved

A new drug, a “NMDA receptor blocker” (Ebixa®), intended to treat symptoms in people with moderate to advanced AD, is available. In trials it stabilized or slowed the decline of cognitive function.

2005: Alzheimer Society Research Funding — $3 million

The Alzheimer Society funds leading scientists, many renowned throughout the world for their work on Alzheimer research. The vast majority of these funds come from public support.

2010: Continued Research

We’ve taken great leaps in the fight against AD in just the past two decades. Breakthroughs — such as vaccines, new drugs and treatments, new diagnostic tools — are on the horizon.

Causes and Origins

An article by Psych Central titled, Causes of Alzheimer’s Disease (2010), indicated that age is the most important known risk factor for AD. The risk of developing the disease doubles every 5 years after age 65 (Nickerson, 2008). Several studies estimate that up to half of all people older than 85 have AD. These facts are significant because of the growing number of people 65 and older (Schoenstadt, 2006). A 2005 Census report estimates that the number of Americans 65 and older will more than double to about 72 million by 2030. Even more significant, the group with the highest risk of Alzheimer’s were those older than 85, and is the fastest growing age group in the United States (Department of Health and Human Services, 2009).

Genetic risk is another factor that a person can’t control. Scientists have found genetic links to the two forms of AD, which are referred to as early-onset and late-onset (Alexander, Larosa, & Alexander, 2010). We can’t do much about our age or genetic profile, but scientists are working hard to understand a variety of other factors that may be involved in the disease. Some scientists are examining the biological bases. This research might lead to the development of drugs that could protect against or block biological processes leading to cognitive decline and AD. Other scientists are studying health, lifestyle, and en­vironmental factors; such as exercise and diet or the control of chronic diseases like diabetes, that may play a role in preventing or slowing AD or cognitive decline. Recent research suggests that maintaining good overall health habits may help lower our chances of developing several serious diseases, including brain diseases such as AD (National Institute on Aging, 2009).

In a meta-analysis conducted by Weih et al., (2009), results clearly showed that increased physical activity when compared to low or no physical activity is associated with a modest reduction of incident AD. Compared with individuals with low or no physical activity, patients with high physical activity or patients reporting physical activity have a 41% reduction of their future risk for developing AD (Weih et al., (2009). Bishop et al. (2009) found that a three-month period of caloric restriction in healthy aged humans was sufficient to improve verbal memory by approximately 20%. Two of the most important ways to prevent AD is good health care and general safety. Getting regular check-ups, exercising, getting adequate rest, and cutting down on alcohol consumption are some of the ways to maintain good health (Living with Alzheimer’s, 2009).

Studies have found that mutations in particular genes increase the likelihood of plaque and tangle formations and, in turn, of AD. Researchers have identified a number of biological factors related to the brain abnormalities seen in AD. One explanation holds that certain substances found in nature, including zinc and aluminum, may produce brain toxicity. Another explanation is the autoimmune theory, which suggests that changes in aging brain cells may trigger an autoimmune response, leading to the disease (Comer, 2010).

Alzheimer Disease Description

Alzheimer’s disease is a neurodegenerative disorder. Alzheimer’s disease is the leading cause of dementia in the elderly, leading to “memory loss” and “cognitive decline” (Nilsson, 2010, p. 741). AD is characterized by a plaque-like substance (the formation of beta-amyloid) that kills brain cells in those afflicted with it (Mucke, 2009). Brain tissue is relentlessly destroyed in a progressive nature that causes an incapacitating loss of mental capacity in individuals suffering from Alzheimer’s. An estimated 2% of the population in the world’s developed nations suffers from AD, with three times that number projected to be afflicted with it by 2054 (Kokjohn & Cooper, 2005).

This would represent over 100 million people suffering from AD worldwide; something that would cripple health-care systems because the disease is so “persistent, disabling and costly” (Mucke, 2009, p. 895). Currently, both genetic and environmental factors are thought to be responsible for AD; though the exact causes of Alzheimer’s “remain a mystery” (Seeds, 2006, p. 20). High-calorie diets that are rich in fat, more sedentary lifestyles, smoking, and other health issues are among environmental factors, while malformed proteins are among the suspected genetic factors of the disease.

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Individuals with AD build up large accumulations of a protein known as beta-amyloid both between and within neurons and in the walls of blood vessels that supply oxygen rich blood to the brain. The exact function of amyloid is not known. However, amyloid forms when a bigger protein is broken into smaller pieces by enzymes. Kokjohn and Cooper (2005) explain that amyloid may protect the brain by sealing blood vessel leaks that occur through “trauma” or “aging” (p. 35). In AD, excessive amyloid deposits build up the “insoluble plaques and degenerating neurons called tangles” that are characteristic of AD (Kokjohn & Cooper, 2005, p. 35). These destructive plaques and tangles form in the area of the brain that is critical to higher-order intellectual functions and memory recall, and the damage is irreversible at the present time.

AD is a fairly difficult disease to diagnose and must be differentiated from a number of other disorders, from depression and schizophrenia to neurodegenerative dementias and Creutzfeldt-Jakob disease. AD most commonly expresses itself as a gradual loss of “episodic memory,” such as forgetting a conversation that occurred the day prior (Mucke, 2009, p. 895). While there is no cure for AD at the current time; treatment options include different groups of medicines, diet and lifestyle changes, and new approaches investigating the use of stem-cell therapy. Because of the challenge of finding Alzheimer disease biomarkers, prevention of the disease is not feasible at this time. This is primarily because preventative treatments, to be effective, would need to begin years, if not decades, before any symptoms of AD would appear (Mucke, 2009, p. 897).

There is no cure, even with the latest medicines; Alzheimer’s patients ultimately suffer a long period of neural cell death that results in irreversible loss of mental capacity. AD is very debilitating in nature. The costs associated with treating Alzheimer’s, and an increasing incidence of AD; finding a means of prevention, means of early detection, an effective treatment, and/or a cure remains imperative for the health-care industry and society.

Differential Diagnosis

One of the most challenging aspects of AD is accurate diagnosis. The American Psychiatric Association (APA) outlines a specific group of criteria for the diagnosis of AD in the Diagnostic and Statistical Manual of Mental Disorders, the DSM-IV (1994). First, several cognitive deficits must be exhibited in those diagnosed with AD, including memory impairment (DSM-IV, 1994). Second, one or multiple of the following deficits must accompany the memory impairment:

Aphasia – A deterioration of language abilities, which can manifest in several ways.

Apraxia – Difficulty executing motor activities, even though movement, senses, and the ability to understand what it is that is being asked are still intact.

Agnosia – An impaired ability to recognize or identify objects, even though sensory abilities are intact.

Executive Functioning Problems – Planning tasks, organizing projects, or carrying out goals in the proper sequence.

(DSM-IV, 1994)

According to the DMS-IV (1994), in order to meet the criteria for AD, the deficits expressed must impact the individual’s ability to hold a job, fulfill domestic duties, and/or maintain social relationships. The deficits must also reflect a profound decline from the individual’s former level of functioning. For a diagnosis of Alzheimer’s, the deficits cannot be due to another medical condition, such as alcoholism or Parkinson’s disease; and, the symptoms cannot happen only during a bout of delirium or be explained better by another psychiatric disorder such as depression or schizophrenia (DSM-IV, 1994). Today, using best practice models of diagnosis; AD can be diagnosed by professionals with more than a 95% accuracy rate (Mucke, 2006, p. 895). Nevertheless, the only method of diagnosing AD with a 100% certainty rate is to perform a detailed post-mortem microscopic examination of the individual’s brain.

Genetic & Environmental Factors

There are genetic and environmental factors thought to be responsible for the development of AD. Most researchers believe AD occurs from the abnormal buildup of harmful proteins in the nervous system, including: AB-peptides, the lipid-carrier protein apolipoprotein E (apoE), the microtubial-associated protein tau, and the presynaptic protein alsp-synuclein (Mucke, 2009, p. 896). All of us make these proteins, but they are usually removed from the brain by clearance mechanisms. AD can be inherited. Some individuals with AD experience early onset because they have inherited “autosomal dominant mutations in genes who protein products – APP, presenilin 1(PS1) or PS2 – are involved in the production of A-beta proteins” (Mucke, 2009, p. 897). Still, the strongest genetic risk factor for the most common form of AD is the APOE 4 gene that encodes the apoE4 lipid carrier (Mucke, 2009). The more common apoE3 and the extremely rare apoE2 and apoE forms of the protein are actually protective against AD (Mucke, 2009). More than 60% of Caucasian patients that are diagnosed with AD carry at least one APOE 4 gene (Mucke, 2009). Those who inherit AD may have two APOE 4 genes, may have inherited an aggressive PS1 mutation; or, they may have inherited one or more minor risk genes combined with environmental factors.

The professional literature makes it clear that there are a number of environmental factors also thought to cause Alzheimer’s; either in combination by themselves or in combination with one or more minor risk genes. Environmental risk factors legitimately linked to AD are low level of education, severe head injury, cerebrovascular disease, diabetes and obesity (Mucke, 2009, p. 896). It remains unclear whether avoiding these risk factors can significantly decrease the chances of developing AD, especially in those with genetic risk factors. Aging, while unavoidable, is also a cause of Alzheimer’s, with the incidence of the illness skyrocketing to 30-33% in those aged 90 and above (Kokjohn & Cooper, 2005). The aging connection may be related to protective mechanisms in the young brain that rid the brain of the excessive buildup of proteins associated with AD. These mechanisms decline with age.

The mechanisms in the young brain that provide such protective factors include higher levels of growth factors, better energy metabolism, and “more efficient mechanisms for clearing misfolded proteins and repairing cells” (Mucke, 2009, p. 896). According to Mucke (2009), inflammation could play a key role in many environmental factors, since “the inflammatory activity of immune cells, particularly macrophages and microglia, and of astrocytes, increases with aging” (p. 896). Aging also makes individuals more prone to environmental risks for development of AD, such as obesity, diabetes, and chronic circulatory conditions.

For over a decade, professionals have supported the excessive amyloid buildup hypothesis as the most common explanation for the development of AD. As Kokjohn and Cooper (2005) points out, “The causes underlying the most common form of Alzheimer’s may be more subtle than the accumulation of a protein leading to brain tissue damage. The amyloid plaque deposits might not even be pathological, but rather part of a defense mechanism to make excess amyloid safe by confining it to a sort of “dump” (p. 36). It is only when deposits in these “dumps” get to extreme levels that dementia becomes apparent. Other theories hypothesize that Alzheimer’s may be more associated with atherosclerosis and dementia, because the same environmental factors that promote atherosclerosis, such as a diet high in calories, saturated fat, and cholesterol, also increases risk of developing dementia (Kokjohn & Cooper, 2005). These theories are encouraging to researchers, healthcare professionals and those suffering from AD. This encouragement stems from the reality that such environmental factors can be eliminated completely or minimized through simple changes in patient lifestyle, such as improved diet, an exercise routine, and pharmacological intervention to adjust fat or cholesterol levels.

Nevertheless, it does appear that malformed proteins are responsible for the formation of the plaque viewed in the brains of patients with AD. One research study took beta-amyloid plaques and injected them into the brains of young mice genetically altered to develop plaques at one year of age (Seeds, 2006). After the injections, the plaques formed more rapidly in the mice, within a few weeks. As one researcher explains, “For the first time we show that the likely seed is beta-amyloid itself” (Seeds, 2006, p. 20). While today’s treatment options offer only moderate and temporary relief of the symptoms associated with AD and while no cure is foreseeable in the near future; the fact that researchers have a much better understanding of both genetic and environmental factors thought responsible for the disease may lead to ways to control the disease at its source.

AD typically develops slowly. The disease can last up to a decade long. AD typically affects all brain functions which include memory, movement, language, behavior, judgment, and abstract reasoning (Mayo Clinic Staff, retrieved 2/10/2010). Some researchers at the Mayo clinic have divided the disease into three stages: mild, moderate, and severe. In the mild stage, a person may experience memory loss, lapse of judgment, and slight changes in personality. Doing familiar things and going to familiar places seems difficult at times. In the middle stage of AD, an individual cannot organize their thoughts and follow instruction. Eventually during this stage, an individual will require help doing simple tasks like putting on their clothes. They may have episodes of incontinence also.

During the last stage, the severe stage, an individual requires help with all of their daily needs. They become unable to walk, talk, eat, and many other daily activities. An individual becomes completely in content and may not speak at all. In most cases, individuals do not recognize family members at all.

Best Practice Models of Diagnosis & Drug Treatment

The difficulty in diagnosing AD and because of no established cure; best practice models of diagnosis and treatment are the surest means of approaching this disease in an effective manner. Best practice models of diagnosis take a multimodal approach to diagnosis of the disease. Hill (2008) reports that the best practice model of diagnosis includes “a team of professionals – including a neurologist, neuropsychologist, geriatrician, and possibly others” (p. 1). Such a team of experts is more able to arrive at an accurate diagnosis. Best practice diagnosis also involves a “total diagnostic workup,” that includes a medical history, imaging procedures, and neuropsychological testing along with other procedures for effective diagnosis of AD (Hill, 2008, p. 1). Only a comprehensive and multimodal diagnosis can clearly differentiate AD from a number of other disorders resembling it.

Best practice models of diagnoses use a combination of tools designed to diagnose and differentiate AD. A careful patient history and of their family is important, as is assessing cognitive function through a variety of neuropsychological tests and radiological modalities. Other causes of dementia must also be eliminated during diagnosis of Alzheimer’s. As researcher Lennart Mucke (2009) explains, “It is crucial to differentiate AD from other neurodegenerative dementias, including fronto-temporal dementia, Lewy-body dementia and Creutzfeldt-Jakob disease” (p. 895). Brain imaging and cerebrospinal fluid (CSF) can also help differentiate Alzheimer’s from these other conditions.

New research studies have contributed to other aspects of diagnosis to differentiate AD. Impaired awareness may be linked to the increase of neuropsychiatric symptoms seen in patients with moderate to severe AD. While this has been established in several studies with moderate to severe AD; researchers Vogel and Waldemar (2010) have investigated if impaired awareness was associated with a “higher frequency” of neuropsychiatric symptoms in patients with early AD. Vogel and Waldemar (2010) found from a study of 321 patients with early AD that “patients with poor insight had significantly more neuropsychiatric symptoms than patients with full insight” (p. 93). Other studies unique in nature have also helped contribute to the multimodal and combined approach to diagnosis of AD.

Nair, Gavett, and Damman (2010) conducted a study of clock drawing test scoring by dementia specialists to determine interrater reliability and diagnostic accuracy. Using three groups of subjects (comparison subjects, mild cognitive impairment patients, and Alzheimer’s patients); researchers found “excellent interrater reliability, sensitivity, and specificity for predicting consensus diagnosis” (Nair, Gavett, & Damman, 2010, p. 85). The outcome shows excellent interrater reliability and sensitivity for “differentiating the mild AD subjects from comparison subjects” (Nair, Gavett, & Damman, 2010, p. 85). The use of amyloid imaging has also shown to be successful in diagnosis of AD; specifically when “factors reported to influence associations between Alzheimer’s pathology and dementia” are linked (Nair, Gavett, & Damman, 2010, p. 85). Roe, Mintun and Williams (2010) conducted research that supports the use of such associations to improve Alzheimer diagnosis. Roe, Mintun and Williams (2010) conclude from their results on Alzheimer’s patients that “factors reported to influence associations between AD pathology and dementia can improve the predictive accuracy of amyloid imaging” (p. 42). A multimodal and combined approach is best suited for accurate Alzheimer’s diagnosis.

Treatment of AD includes three different groups of medicines that have a temporary effect on symptoms of the disease. These include: 1) inhibitors or acetylcholinesterase; 2) an antagonist of a receptor for the neurotransmitter glutamate; and, 3) drugs that control depression and behavioral abnormalities (Mucke, 2009, p. 896.). Medications include memantine, donepezil and galantamine; all three of which have been shown to be efficacious in “slowing memory loss in individuals with AD” (Age, 2010). Most of the recent research has focused on the use of different medications to help treat the symptoms of the disease. “These drugs include a wide variety of compounds aimed at improving cerebral blood flow or levels of various neurotransmitters. Some of the drugs, such as tacrine (Cognex, doneprzil (Aricept), galantamine (Reminyl), and rivastigmine (Exelon) have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of AD.” (Cavanugh & Blanchard-Fields, p.138, 2006). Although all of the drugs show some improvement, none of the drugs have shown significant improvement in a wide variety of patients. Changes in diet and lifestyle are also employed in order to offset environmental factors thought to be associated with AD. These include exercise, nutrition and social interaction (Age, 2010). Adding to the costs of treating Alzheimer’s is the fact that any treatment approach requires careful monitoring by family and professionals.

According to the Canadian Medical Association Journal (2008), severe AD requires frequent monitoring and the use of antipsychotic drug therapy is “occasionally necessary despite the inherent risks” (p. 1279). Cholinesterase inhibitors and memantine have showed to be useful only for “select patients,” while “all pharmacological approaches require careful monitoring and periodic reassessment to determine whether continued treatment is necessary” (Diagnosis, 2008, p. 1279). Because of this requirement and the significant and often crippling costs associated with caring for Alzheimer’s patients; the use of caregiver support and community resources is often necessary. Neuropsychiatric symptoms are most often treated with non-pharmacological approaches during early onset, but severe agitation, aggression, and psychosis are potential dangers to the patient and caregivers and are often treated with antipsychotic drugs (Diagnosis, 2008). However, these drugs include the risk of increased cerebrovascular events and even death.

Scientists have a much greater understanding of the genetic and biochemical pathways of the amyloid that is linked to AD; new methods of treatment may one day be able to cure the disease at its source. For instance, enzymes may be able to stop toxic levels of amyloid production or amyloid deposits may be removed through vaccination or other methodologies. Nilsson (2010) argues that the “multifactorial causes of AD offer a variety of possible targets for gene therapy, including two neurotrophic growth factors, nerve growth factor and brain-derived neurotrophic factor” (p. 741). Because of the potential devastation to the health-care system and the significant threat to society, from the predicted significant increase in AD; it is likely such alternative and unique treatment options will continue to be developed by professionals as more understanding of the causes of this disease are discovered.

Diagnosing with Radiology Modalities

At the present time, there is no one known cause for AD. There have been many case studies to try and figure out the exact cause and/or causes so that families might be able to prevent the disease from taking over the minds of loved ones. In order for a person to be diagnosed with AD accurately, in the past an autopsy would need to be performed after death. Although, many clinicians try to diagnose the disease without performing the accurate and adequate test to rule out all other possible medical illnesses, many general practitioners miss diagnose the disease. “The clinical diagnosis of AD consists of carefully noting the history of symptoms, documenting the cognitive impairments, conducting a general physical exam and neurological exam, performing laboratory tests to rule out other disease, obtaining a psychiatric evaluation, performing neuropsychological tests, and assessing functional abilities”, (Cavanaugh & Blanchard-Fields, 2006). In order for a physician to rule out physical illness, numerous medical exams prior to any psychological or other follow up test need to be conducted. Radiological modalities such as Magnetic Resonance Imaging (MRI), Computerized Tomography (CT), Nuclear Medicine and Positron Emission Scans are key diagnostic tools in detecting, diagnosis and prognosis of AD.

The brain is the most powerful organ in the body and weights about three pounds. The brain consists of three main parts:

The cerebrum fills up most of your skull. It is involved in remembering, problem solving, thinking, and feeling. It also controls movement.

The cerebellum sits at the back of your head, under the cerebrum. It controls coordination and balance.

The brain stem sits beneath your cerebrum in front of your cerebellum. It connects the brain to the spinal cord and controls automatic functions such as breathing, digestion, heart rate and blood pressure. (Alzheimer’s Association, 2010)

In an Alzheimer’s brain the cortex shrivels up, damaging areas involved in thinking, planning and remembering. The hippocampus has significant shrinkage, which plays a key role in formation of new memories. The ventricles of the brain, the fluid filled space, grow larger. These changes in the brain are due to the buildup of the plaque and tangles. To help physicians give a firm diagnosis of dementia and/or AD, non-invasive brain imaging and cognitive status are crucial to patient care. The two most popular brain imaging modalities are MRI and PET imaging. MRI is more cost effective than PET imaging.

An MRI scan of the brain will cost a patient about $1,200 to $1,800, while a PET scan will cost about $4,000 (Rapoport, 2000). MRI’s uses magnetism and radio waves to visualize what is inside the body. MRI’s usually consist of two to six imaging sequences, each lasting from two to fifteen minutes depending upon the area of interest. Each sequence can produce an image of the area of interest in several planes or image slices or cross sections. MRI’s are able to detect certain diseases much earlier than other medical imaging technologies, therefore often lowering diagnostic work-up and aid in the early diagnosis or prognosis of AD.

MRI scans can detect shrinkage in specific regions of the mid-brain attacked by AD accurately diagnose the neurodegenerative disease, even before symptoms interfere with daily function, a study by the Florida AD Research Center (ADRC) in Miami and Tampa found. The study, reported earlier this month in the journal Neurology, adds to a growing body of evidence indicating MRI brain scans provide valuable diagnostic information about AD. The findings are important in light of many new disease-modifying drugs in trials — treatments that may prevent mild memory loss from advancing to full-blown dementia if administered early enough.

“We advocate, based on these findings, that the criteria for the diagnosis of AD should include MRI scans,” said the study’s lead author Ranjan Duara, MD, medical director of the Wien Center for AD and Memory Disorders at Mount Sinai Medical Center who is affiliated with the University of Miami Miller School of Medicine and University of South Florida College of Medicine. “By incorporating MRIs into the assessment of patients with memory problems, early diagnosis can be standardized and done far more accurately.” “This study demonstrates that MRI brain scans are accurate enough to be clinically useful, both in diagnosing AD itself at an early stage and in identifying people at risk of developing Alzheimer’s,” said Florida ADRC Director Huntington Potter, PhD, a neuroscientist at the Byrd Alzheimer’s Center and Research Institute, University of South Florida. University of South Florida Health (2008, December 23).



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