Scientists are hopeful that discoveries in these areas will inform new ways to diagnose, treat, or even prevent AD. Neurotransmitter depletion is also implicated in the disease process and represents another area of study. Acetylcholine is a neurotransmitter that is consistently deficient in patients with AD; the deficiency is associated with memory loss and loss of capacity for attentiveness. Other neurotransmitters that are reduced in patients with AD include serotonin, gamma- aminobutyric acid (GABA), somatostatin, and norepinephrine. Current drug therapies focus on these neurotransmitter depletions. Growth factors are important for regulating many cellular processes; their depletion, especially the depletion of brain-derived neurotrophic factor (BDNF), which is neuroprotective in nature, appears to be implicated in the pathology of AD.
may run in families led to the identification of mutations on chromosome 14 (presenilin-1 gene), chromosome 1 (presenilin-2 gene), and chromosome 21 (amyloid precursor protein gene), all of which cause abnormal proteins to be produced. Even if only one of these genes contains a mutation, an individual will almost inevitably develop early-onset AD. Genetic research into late-onset AD has identified a region on chromosome 19 that may be involved in the development of the disease. The protein apolipoprotein E (ApoE) is associated with beta- amyloid plaques. The gene that produces ApoE is located in a region of chromosome 19 that was pinpointed by geneticists, suggesting that one form of this gene (ApoE-4) is a risk factor for late-onset AD; however, even inheriting ApoE-4 from both parents does not translate to definitive development of AD and some individuals with AD may not have inherited ApoE-4 from either parent. Understanding the genetics and implications in the changes in protein structures is a major focus of AD research.
RISK FACTORS FOR ALZHEIMER’S DISEASE
with these disparities do not appear to be genetic and may instead be explained by differential rates of conditions such as hypertension and diabetes among the groups, socioeconomic disparities associated with education and access to medical care, and underdiagnosis in these ethnic subgroups. ● History of head trauma: A significant brain injury or repeated minor brain injuries (concussions) have been linked to increased risk for AD or AD-like dementia (i.e., chronic traumatic encephalopathy). Increasingly, evidence demonstrates the cognitive protective effect of a lifetime of physical activity and mental engagement (Phillips, 2017), and neuroimaging studies have confirmed some of the neural plastic effects of both active lifestyles and activity interventions. Expansion or diminished atrophy of the prefrontal cortex and hippocampal brain regions in individuals who engage in high levels of physical activity have been demonstrated (Erickson, Weinstein, & Lopez, 2012). While a lifetime of physical activity and fitness is ideal, it is never too late to begin a training or activity regimen. Targeting those with a genetic risk for AD or those with mild cognitive impairment (which often transitions to dementia) for activity interventions may be promising for impacting the course of disease progression (Öhman, Savikko, Strandberg, & Pitkälä, 2014; J. C. Smith et al., 2014). Rehabilitation professionals who are committed to health and wellness have a responsibility to educate colleagues in health care, and patients or clients and their families, about the power of physical activity. Physical therapists, with their expertise in movement systems and activity prescription, are uniquely positioned to have a significant impact on the mobility, functionality, and health of older adults.
AD is a multifactorial disease with a long list of risk factors. The major risk factors include the following: ● Age: Age is the most strongly established risk factor for AD. The older a person gets, the greater the risk for the disease. The risk doubles every 5 years after age 65. It is relevant to mention that early-onset AD (prior to age 65) accounts for about 5% of AD cases and is usually diagnosed in individuals in their 40s and 50s. ● Genetics: As mentioned previously, for early-onset AD, mutations have been identified on chromosomes 14, 1, and 21; for late-onset AD, chromosome 19 has been identified as a source for gene ApoE-4, which is associated with an increased risk of AD. ● Vascular disease: Impaired blood flow to the brain is the cause of vascular dementia and is contributory to AD. Systemic vascular problems that contribute to heart disease, such as atherosclerosis and hypertension, may be implicated in AD. ● Metabolic conditions: Diabetes and obesity have been associated with increased risk of AD. ● Years of education: Lower educational levels are associated with a greater likelihood of AD. Speculation regarding the role of education includes an increased cognitive reserve to compensate for brain changes that could lead to dementia among those with higher levels of education, as well as decreased access to medical care among persons with lower educational attainment, which is inexorably linked with socioeconomic status. ● Ethnicity: Although the majority of older Americans with dementia are Caucasian, research suggests that older African Americans and Hispanics are more likely to be afflicted with dementia than older Caucasians. Factors associated
DIAGNOSIS OF ALZHEIMER’S DISEASE
or her family know the diagnosis, the more time they have to make future arrangements, handle financial matters, establish a durable power of attorney, deal with other legal issues, create a support network, and make plans to join a research study. However, because there is no cure or even a substantially effective treatment for AD, some individuals and their families intentionally delay a diagnostic workup for as long as possible, thinking they would rather be unsure of the diagnosis than to know definitively that the individual has a condition for which there is no cure. AD and issued new criteria and guidelines for diagnosis. These core clinical criteria identify three stages of AD: preclinical, mild cognitive impairment (MCI) due to AD, and dementia due to AD (Jack et al., 2011). These criteria, as mentioned, highlight that Alzheimer’s disease begins before dementia is apparent in the mild or early stage and can be diagnosed by biomarkers
The diagnosis of AD and related neurocognitive disorders is important for several reasons. Most importantly, many conditions that cause symptoms that mimic those of AD may be treatable. Prompt identification and management of a treatable condition that mimics AD may totally resolve the problem. The Alzheimer’s Association has championed a campaign for early detection and diagnosis of AD. Early diagnosis may give individuals with AD an opportunity to take medications that may slightly slow the progression of symptoms during the early stages. Pragmatically, the sooner an individual with AD and his Diagnostic criteria and guidelines Currently, there is no definitive test to diagnose AD, and there continues to be some disagreement within both the research and clinical worlds as to the optimal diagnostic criteria for AD (Morris et al., 2014). In 2011, the NIA, the Alzheimer’s Association, and experts from around the world synthesized information on the pathophysiological and clinical aspects of
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