* If you want to update the article please login/register
As the most common form of dementia and the sixth - leading cause of death in the US, Alzheimer's Disease is not foreign to Americans. Many in the US know someone battling a disease or disease that doctors are still continuing to understand. While the majority of previous research has been focused on treatment, researchers are beginning to shift their attention toward prevention. In recent virtual presentation in partnership between Alzheimers Associations Michigan chapter and Michigan Alzheimers Disease Research Center, Bruno Giordani, ph. D, Professor in departments of psychiatry, Neurology and psychology, discussed science behind Alzheimers Disease as well as the latest research from the most recent Alzheimers Association International Conference. According to Giordani, new research findings led to an entire change in emphasis of research, as more evidence was released to support risk - reducing tactics over later treatment. Alzheimer's Disease involves memory loss, confusion and spatial difficulties, which all come down to the existence of amyloid plaques. Amyloid plaques, or hallmarks of Alzheimer's Disease, as Giordani calls them, are clumps of misshapen proteins that form between nerve cells and essentially act as roadblocks for memory. Cell death also occurs in specific areas of the brain, such as the hippocampus, which is critical for areas of cognition like memory and spatial navigation. Scientists are gaining better understanding of the course of Alzheimer's Disease, which progresses from prodromal or pre - clinical period to mild cognitive impairment and then dementia. Knowledge of this path, as well as earlier tracking of amyloid, has given doctors the chance to work toward risk diagnosis and preventative medications, as opposed to later treatment of disease. Id usually tell you about all the exciting new amyloid drugs present at AAIC meeting; amyloid busters that we can apply to get rid of amyloid in the brain. Frankly, these have not worked out as expect, Giordani explain. Researchers are now attempting to disrupt the process even earlier, before amyloid plaques form and begin to disturb memory. In recent discussion with Giordani, he highlighted news that Biogen, American biotechnology company, completed submission to the US Food and Drug Administration for review of aducanumab, investigational treatment for Alzheimer's Disease that targets amyloid in the brain in hopes of reducing its buildup. If approve, aducanumab would become the first therapy to reduce clinical decline of Alzheimer's Disease and would also be the first therapy to demonstrate that removing amyloid beta results in better clinical outcomes, which could be significant news for Alzheimer's treatment. Researchers are also examining how parts of the body, other than the brain, may play a role in disease development. Studies have looked into the effect of various medications individuals are already taking, such as insulin, and are finding promising results. Study looking at inhaled insulin show some cognitive and amyloid - tau distribution improvements, but the type of inhaler seems to make a big difference. Other approaches include studying gingivitis and other markers of inflammation, which Giordani says may help track disease process earlier on as well.
* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.
Anti - amyloid aggregation agents hypothesis that aggregation leads to toxic oligomeres has driven research into studying compounds that could prevent this aggregation. The only aggregation inhibitor reaching phase III is synthetic glycosaminoglycan 3 - amino - 1propaneosulfonic acid. It is designed to interfere with the binding of glycosaminoglycanes and. Disappointing results of the North American phase III Trial in year 2007 have led to the discontinuation of the European phase III Trial. Nevertheless, 3APS will now be commercialized as a branded nutraceutical. However, recent data suggest that tramiprosate promotes abnormal aggregation of tau protein in neuronal cells. These results emphasize the importance of testing potential drugs for treatment of AD on both types of pathology. Another molecule undergoing testing is colostrinin, proline - rich polypeptide complex derived from sheep colostrum. Colostrinin inhibits aggregation and neurotoxicity in cellular assays and improves cognitive performance in animal models. Although the phase II trial demonstrated modest improvements in Mini Mental State Evaluation scores for patients with Mild AD over a treatment period of 15 months, this beneficial effect was not sustained during additional 15 months of continued treatment. Another compound named scyllo - inositol is able to stabilize oligomeric aggregates and inhibit toxicity in mouse hippocampus. An 18 - month, randomize, double - blind, placebo - control, dose - ranging, safety and efficacy study of oral scyllo - inositol in participants with mild to moderate AD has been carried out by Transition Therapeutics / Elan. Long - term follow - up class II Study in subjects with AD provides insufficient evidence to support or refute the benefit of ELND005. Primary Clinical efficacy outcomes were not significant. Safety and cerebrospinal fluid biomarker results will guide selection of optimal dose for future studies, which will target earlier stages of AD. Drugs interfering with metals, zinc and copper are both involved in the aggregation of A42. Several chelators of Zn / Cu have been shown to inhibit aggregation in vitro and in animal studies. Pbt2 is a second - generation 8 - OH quinoline metal - protein - attenuating compound that affects Cu2 + - mediate and Zn2 + - mediate toxic oligomerization recent phase IIA Study concluded that the safety profile is favorable for ongoing development of PBT2. Effect on putative biomarkers for AD in CSF but not in plasma suggests central effect of drug on metabolism. Cognitive efficacy was restricted to two measures of executive function. In post hoc analysis, cognitive, blood marker and CSF neurochemistry outcomes from the trial were subject to further analysis. Ranking responses to treatment after 12 weeks with placebo, PBT2 50 mg and PBT2 250 mg reveal that proportions of patients showing improvement were significantly greater in the PBT2 250 mg group than in the placebo group. These findings further encourage larger - scale testing of PBT2 for AD. It is generated through proteolytic processing of transmembrane peptide APP. Apps can be cloven by two competing proteases, Secretase and Secretase. Only cleavage by Secretase, followed by - Secretase cleavage, which in AD is the dominant pathway, will lead to production of A40 and A42.
* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.
Developing new medications is a slow and painstaking process. Pace can be especially frustrating for people with Alzheimer's and their families who are waiting for new treatment options. To help accelerate Discovery, Coalition Against Major Diseases, alliance of pharmaceutical companies, nonprofit foundations and government advisers, has forged a first - of - its - kind partnership to share data from Alzheimer's Clinical trials. Camd has also collaborated with the Clinical Data Interchange Standards Consortium to create Data Standards. Researchers anticipate that these Data Standards and sharing of data from more than 6 500 study participants will speed development of more - effective therapies.
* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.
Current Alzheimer's treatments temporarily improve symptoms of memory loss and problems with thinking and reasoning. These Alzheimer's treatments boost the performance of chemicals in the brain that carry information from one brain cell to another. However, these treatments don't stop the underlying decline and death of brain cells. As more cells die, Alzheimer's Disease continues to progress. Experts are cautiously hopeful about developing Alzheimer's treatments that can stop or significantly delay progression of Alzheimer's. Growing understanding of how disease disrupts the brain has led to potential Alzheimer's treatments that short - circuit basic disease process. Future Alzheimer's treatments may include a combination of medications, similar to how treatments for many cancers or HIV / AIDS include more than a single drug. Following treatment options are among strategies currently being study.
Currently, there is lack of, and great need for, effective treatments to prevent and slow progression of AD. The last 30 years of research into mechanisms of AD has presented numerous treatment strategies that target underlying causes of neurodegeneration, with the majority of this work focussing on targeting cascades which prevent accumulation of toxic amyloid aggregates. Despite many critical discoveries and promising directions, there is healthy skepticism about whether targeting pathology alone is effective for modifying disease progression in light of many failures in late - phase clinical trials. Further understanding of disease mechanisms and careful considerations of clinical trial design is providing important insights that will aid in combating AD. This portion of the review pertains to treatment strategies that modify progression of AD, from molecular treatments to lifestyle therapies, stretching from pre - clinical to clinical trials.
Recent developments have brought about a staggering array of research approaches that are offering bold new ways to study human brain aging and are yielding profuse and meaningful human data. These techniques include: several human - base Models focus on use of patient - derived cells, such as induced pluripotent stem cells and neuronal and glial cultures, multiple omic technologies resulting from overall analyses of biological samples by high - throughput analytical approaches and databases, computational analytical approaches and novel Neuroimaging readouts. Give need to integrate huge amounts of incoming data, comprehensive multi - scale and systems biology approaches are becoming fundamentally important. These approaches must take into account all different levels of biological complexity, thereby allowing for elucidation of Disease - related Adverse outcome pathways, as already envisioned in toxicology and proposed for AD Research. Within this new Framework, it is becoming increasingly possible to not only determine the effects of exposure to give compound but also to investigate how these effects are induce. Defining which signaling pathways are perturbed at early stages of AD might help predict long - term effects and sequelae. For this reason, multiscale AOPs should become the core of a new paradigm in AD research. Investigating AD - related multiscale AOPs could allow researchers to link environmental and genetic causes with outcomes at individual / body level. The number of cellular in vitro Models of AD and human - base methods can already take into account different levels of biological complexity. For example, iPSCs have been widely applied in AD Research and can be used to: assess clinical candidate drugs on human brain cell types; conduct phenotypic screening of compounds that modulate or normalize disease phenotype; conduct target - base screening if candidate genes are identify; compare genetically - diverse panels; or select or stratify participants of clinical trials base on their genetic backgrounds and / or phenotypic traits. Moreover, human - base Intervention trials focus on nutrition, physical activity, and Cognitive training are particularly relevant to preventing AD and Cognitive decline. These trials have proven to be the most effective strategies to reduce AD symptoms. In order to stimulate creation of multifactorial approaches to AD, global efforts have been made to improve access and discussion online for researchers. In recent years, common platforms, such as CLIR, Develop at Mayo Clinic, have been shown to be suitable to create groups of interest and propose multidisciplinary team approaches, allowing comparisons among different sub - populations, different ages and different treatments. At clinical level, databases, such as the Laboratory of Neuroimaging - Image Data Archive, provide user access to de - identify data from positron emission tomography, magnetic resonance Imaging, Cognitive Data sets and biomarkers. These interfaces represent a large step forward in maximizing the impact of this data. As alternatives to use of traditional mammalian species, some non - mammalian / non - vertebrate models, such as Dictyostelium discoideum, have also been applied to undertake new directions in Basic Research and define the role of previously unexplored proteins / molecules. Taking into account their biological limitations, these non - mammalian models are relatively easy to handle, cost effective, and can be manipulated to express AD - related human genes / proteins.
At Alzheimers Drug Discovery Foundation, nonprofit charity based in New York City, diversity is reflected in research projects being funded there. We were really seeing every type of different approach to Alzheimer's disease and related dementias, said Lauren Friedman, director of scientific affairs at ADDF. Areas being explored include vascular system, epigenetics, neuroprotection, synaptic health, immunity and inflammation, and metabolic dysfunction, among others. Neuroinflammation and proteostasis, or management of proteins within cells, are trending areas of research in ADDFs portfolio. Researchers investigating proteostasis would like to find ways to boost cells garbage disposal systems, which identify misfolded, clumping proteins and chew them up for recycling. Like other companies, Novartis is exploring targets in inflammation and the immune system. Dolmetsch notes that the field has just begun to sort through all of the activated inflammatory cells that show up in Alzheimer's patients brains and to characterize their various states of activity and exhaustion. Exhaust microglia, custodians of the brain, for example, start pumping out cytokines to call up more cells, which leads to chronic inflammation. Such inflammation might be fine for temporary response to injury in, say, finger. But as a chronic state, it doesnt work so well in your brain, Dolmetsch say. For neuroinflammation projects, Novartis looks for scientists who have training with overlaps between Neuroscience, immunology, and bioinformatics. The George & Anne Ryan Institute for Neuroscience at University of Rhode Island in Kingston investigates underexplored factors in brain health, including roles of vasculature, immunology, and neuroinflammation as well as lifestyle and environment in Alzheimers disease and other neurodegenerative disorders. Behavioral neuroscientist John Robinson works on rodent models of how exercise might play a role in modifying or preventing Alzheimers. The biggest risk factor for Alzheimers is age, he note, which is, unfortunately, not modifiable. But we often say that what is good for the heart is good for the brain. Another booming area of Alzheimers research is development of biomarkers and diagnostic tests to monitor disease presence and progression. Radioactive positron emission tomography tracers enable physicians to image and measure amyloid and tau proteins in the brains of living patients. Other biomarkers can be measured precisely from collecting cerebral spinal fluid. However, both types of tests are invasive, and PET scans are expensive. We need blood tests like we have for cholesterol that can be done in any doctor's office quickly and inexpensively, says Friedman. To spur such development, ADDF has teamed up with Bill Gates and other philanthropists to fund the Diagnostics Accelerator program. Friedman says the program anticipates awarding about $10 million in the first round of funding. So far, it has funded projects for blood tests and tests that detect amyloid or vascular changes in the retina, and is reviewing applications for digital tests that use smartphones or tablets to monitor disease signs or symptoms.
Accelerating Research and Clinical Development efforts and bringing DMTs to market sooner would have significant impact on future societal burden of AD. Under current conditions, only drugs currently in late Phase 1 or later could be ready by 2025, and only if studies progress optimally. If pipeline attrition rates remain high, it is likely that only a few compounds could possibly reach this milestone. There is great need to reduce the time and risk of AD Drug Development to reach the 2025 goal. We have discussed key areas by which we can address this challenge in trial design; better trial infrastructure; Disease registries of well - characterized patient cohorts to help with fast / timely enrollment of appropriate study population; validating biomarkers to better detect disease, determine risk and monitor disease as well as predict Disease response; more sensitive Clinical assessment tools; and faster regulatory Review. To implement change requires efforts to build awareness, educate and foster engagement; financial commitment to increase funding for both basic and Clinical Research; collaboration to reduce fragmented environments and systems, to increase learning from successes and failures, to promote data standardization and thus increase wider data sharing; and greater depth of understanding of AD at basic biology level and speedy translation of New Knowledge into Clinical Development. Improve mechanistic understanding of disease development and progression is critical to more efficient AD Drug Development and will LEAD to improve therapeutic approaches and targets. More effective tools, such as biomarkers and sensitive cognitive assessments, and more appropriate selection of participants will LEAD to improved Clinical Trials. Effort required to advance Drugs from bench to bedside is poorly understood by most AD stakeholders, and education regarding complexities, long time frames, and expense of AD Drug development is critical. As these steps are put in place and plan comes to fruition, it can be predicted that momentum will build, process will be self - sustaining, and the path to 2025, and beyond, will become clearer.
For more than 30 years, strategies to support family caregivers of people with Dementia have been developed and evaluate. The types and focus of these strategies are summarized in Table 9. 347 409 in general, goal of interventions is to improve the health and wellbeing of Dementia caregivers by relieving negative aspects of caregiving. Some also aim to delay nursing home admission of people with Dementia by providing caregivers with skills and resources to continue helping their relatives or friends at home. Specific approaches used in various interventions include providing education to caregivers, helping caregivers manage dementiarelated symptoms, improving social support for caregivers and providing caregivers with respite from caregiving duties. According to publication on Dementia caregiver interventions that reviews seven metaanalyses and 17 systematic reviews of randomized controlled trials, following characteristics distinguish interventions that are effective: Family caregivers are actively involved in Intervention, in contrast to passively receiving information; Intervention is tailored and flexible to meet changing needs of Family caregivers during course of relative's Dementia; and Intervention meets need not only of caregivers, but of people living With Dementia As well. 410 2012 Report examines randomize, controlled studies of caregiver interventions and identifies 44 interventions that benefit individuals with Dementia as well as caregivers. More such interventions are emerging each year. 411 - 416 metaanalysis examining components of Dementia caregiver interventions that are most beneficial found that interventions that initially enhance caregiving competency, gradually address care needs of person with Dementia, and offer emotional support for loss and grief when need appear most effective. 417 interventions for Dementia caregivers that have demonstrated efficacy in scientific evaluations have been gradually implemented in the community, but are still not widespread or available to all family caregivers. 418 - 432 When interventions are implement, they are generally successful at improving how caregiver services are deliver, and have the potential to reach large numbers of families while also helping caregivers cope with their responsibilities. 433 in One example, researchers utilize agile implementation process to more rapidly select, localize, evaluate and replicate collaborative Care model for Dementia Care. This care model has successfully operated for nearly a decade in the Indianapolis Health Care system. 434 Other efforts have attempted to broaden the reach and accessibility of interventions for Dementia caregivers through use of technologies, 435 - 442 While others integrate evidencebased Dementia Care interventions into communitybased, - longterm service programs. 443 in 2019, National Institute on Aging award funding to create NIA imbed Pragmatic AD / ADRD Clinical Trials Collaboratory. The collaboratory includes experts from more than 30 top research institutions and will support up to 40 pilot trials to test nondrug, carebased - interventions for people living with Dementia in the next five years. The goal of IMPACT is to expedite timeline of research implementation in realworld settings to improve care for people living with Dementia and their caregivers.
Although there are more nonHispanic whites living with Alzheimer's and other dementias than any other racial or ethnic group in the United States, older black / African Americans and Hispanics / Latinos are disproportionately more likely than older whites to have Alzheimer's or other dementias. 16 17 236 - 239 Most studies indicate that older black / African Americans are about twice as likely to have Alzheimer's or other dementias as older whites. 18 19 209 Some studies indicate older Hispanics / Latinos are about one and onehalf times as likely to have Alzheimer's or other dementias as older whites. 8 19 240 241 However, Hispanics / Latinos comprise a very diverse group in terms of cultural history, genetic ancestry and health profiles, and there is evidence that prevalence may differ from one specific Hispanic / Latino ethnic group to another. 242 243 The higher prevalence of Alzheimer's dementia in minority racial and ethnic groups compared with whites appears to be due to higher incidence of dementia in these groups. 244 Variations in medical conditions, healthrelated behaviors and Socioeconomic Risk factors across racial groups likely account for most of the differences in risk of Alzheimer's and other dementias. 239 Despite some evidence that the influence of genetic risk factors on Alzheimer's and other dementias may differ by race, 80 82 245 genetic factors do not appear to account for large differences in prevalence or incidence among racial groups. 244 246 Instead, health conditions such as cardiovascular disease and diabetes, which are associated with increased risk for Alzheimer's and other dementias, are believed to account for these differences, as they are more prevalent in black / African American and Hispanic / Latino people. 247 248 Socioeconomic characteristics, including lower levels and quality of education, higher rates of poverty, and greater exposure to adversity and discrimination, may also increase risk in black / African American and Hispanic / Latino communities. 80 247 - 249 Some studies suggest that differences based on race and ethnicity do not persist in rigorous analyses that account for such factors. 135 187 244 There is evidence that missed diagnoses of Alzheimer's and other dementias are more common among older black / African Americans and Hispanics / Latinos than among older whites. 250 251 based on data for Medicare beneficiaries aged 65 and older,. It has been estimated that Alzheimer's or another dementia had been diagnosed in 10. 3% of whites, 12. 2% of Hispanics / Latinos and 13. 8% of black / African Americans. 252 Although rates of diagnosis were higher among black / African Americans than among whites, according to prevalence studies that detect all people who have dementia irrespective of their use of the health care system, rates should be even higher for black / African Americans. There is fewer data from populationbased cohort studies regarding national prevalence of Alzheimer's and other dementias in racial and ethnic groups other than whites, black / African Americans and Hispanics / Latinos. However, study examining electronic medical records of members of large health plans in California indicates that dementia incidence determined by presence of dementia diagnosis in members ' medical records was highest in black / African Americans, intermediate for Latinos and whites, and lowest for Asian Americans.
It is difficult to determine how many deaths are caused by Alzheimer's Disease each year because of the way causes of death are record. According to data from the Centers for Disease Control and Prevention, 122 019 people died from Alzheimer's Disease in 2018, latest year for which data is available. 281 CDC considers a person to have died from Alzheimer's if the death certificate lists Alzheimer's as the underlying cause of Death, defined as disease or injury which initiates train of events leading directly to death. 282 in the United States, Alzheimer's Disease is counted as a cause of Death that can be ranked against other leading causes of death such as cancer and heart disease, but deaths due to other types of clinically diagnosed dementia are not ranked in this manner. The number of deaths from dementia of any type is much higher than the number of reported Alzheimer's deaths. In 2018, some form of dementia was officially recorded as the underlying cause of death for 266 957 individuals. 281 283 Therefore, number of deaths from all causes of dementia, even As list on death certificates, is more than twice as high as the number of reported Alzheimer's deaths alone. To add further complexity, vast majority of death certificates listing Alzheimer's Disease or dementia as the underlying cause of death are not verified by autopsy, and research has shown that about 30% of those diagnosed with Alzheimer's dementia during life do not in fact have dementia due to Alzheimer's Disease, but have dementia due to another cause. Therefore, underlying cause of Death list as Alzheimer's Disease may not be accurate. In this section, deaths from Alzheimer's Disease refers to what is officially reported on death certificates, with the understanding that person filling out the report believe dementia due to Alzheimer's Disease was the underlying cause of death, usually without pathologic confirmation. Severe dementia frequently causes complications such as immobility, swallowing disorders and malnutrition that significantly increase the risk of serious acute conditions that can cause death. One such condition is pneumonia, which is the most commonly identified immediate cause of death among older adults with Alzheimer's or other dementias. 284 285 One autopsy study found that respiratory system diseases were the immediate cause of death in more than half of people with Alzheimer's dementia, followed by circulatory system disease in about quarter. 285 Death certificates for individuals with Alzheimer's often list acute conditions such as pneumonia as the primary cause of death rather than Alzheimer's. 286 - 288 As a result, people with Alzheimer's dementia who die due to these acute conditions may not be counted among the number of people who die from Alzheimer's Disease, even though Alzheimer's Disease may well have caused acute condition list on the death certificate. This difficulty in using death certificates to determine the number of deaths from Alzheimer's and other dementias has been referred to as blur distinction between death with dementia and death from dementia.
Eightythree percent of help provided to older adults in the United States comes from family members, friends or other unpaid caregivers. 308 Nearly half of all caregivers who provide help to older adults do so for someone with Alzheimer's or another dementia. 309 More than 16 million Americans provide unpaid care for people with Alzheimer's or other dementias. 12 It is important to note that the number of caregivers for people with Alzheimer's or other dementias is calculated using a model that incorporate, in part, data from 2009, most recent date for which data is available. There are indications that over the past decade, number of Family Caregivers for all older Americans may have decline. The Alzheimer's Association is examining new data and recently released statespecific Data on dementia Caregivers and is working with experts to revise the model to take into account these recent trends. Preliminary evaluation indicate that, compared with the past, there are fewer family caregivers in total, and each individual caregiver is experiencing greater burden by providing significantly more hours of care. If this preliminary analysis hold, future estimates of the number of Alzheimer's and dementia caregivers nationally and for each state will be lower than current estimates. In 2019, caregivers of people with Alzheimer's or other dementias provide an estimate of 18. 6 billion hours of informal assistance, contribution to a nation valued at nearly $244 billion. This is approximately 47% of the net value of Walmart's total revenue in 2019 310 and 11 times total revenue of McDonald's in 2018. 311 total lifetime cost of care for someone with dementia was estimated at $357 297 in 2019 dollars. Seventy percent of the lifetime cost of care is bear by Family Caregivers in the forms of unpaid caregiving and out‐of‐pocket expenses for items ranging from medications to food for people with dementia. 312 313 Current estimates of lifetime costs of care may underestimate the impact of relative's dementia on family caregivers ' health and workplace productivity. The three main reasons caregivers provide care and assistance to person with Alzheimer's or another dementia are a desire to keep family members or friends at home, proximity to person with dementia and caregiver's perceive obligation to person with dementia. 13 Caregivers often indicate love and a sense of duty and obligation when describing what motivates them to assume care responsibilities for relative or friend living with dementia. 315 Individuals with dementia living in the community are more likely than older adults without dementia to rely on multiple unpaid caregivers; 30% of older adults with dementia rely on three or more unpaid caregivers, whereas 23% of older adults without dementia rely on three or more unpaid caregivers. 316 Only a small percentage of older adults with dementia do not receive help from family members or other informal care providers. Of these individuals, nearly half live alone, perhaps making it more difficult to ask for and receive informal care.
Memory Problems are typically one of the first signs of cognitive impairment related to Alzheimer's Disease. Some people with memory problems have a condition called mild cognitive impairment. In MCI, people have more memory problems than normal for their age, but their symptoms do not interfere with their everyday lives. Movement difficulties and problems with sense of smell have also been linked to MCI. Older people with MCI are at greater risk of developing Alzheimers, but not all of them do. Some may even go back to normal cognition. First symptoms of Alzheimers vary from person to person. For many, decline in non - memory aspects of cognition, such as word - finding, vision / spatial issues, and impaired reasoning or judgment, may signal very early stages of Alzheimers Disease. Researchers are studying biomarkers to detect early changes in the brains of people with MCI and in cognitively normal people who may be at greater risk for Alzheimers. Studies indicate that such early detection is possible, but more research is needed before these techniques can be used routinely to diagnose Alzheimer's Disease in everyday medical practice.
Among Medicare beneficiaries with Alzheimer's or other dementias, Black / African Americans had the highest Medicare payments per person per year, while whites had the lowest payments. The largest difference in payments was for hospital care, with Black / African Americans incurring 1. 7 times as much in hospital care costs as whites. 291 in study of Medicaid beneficiaries with diagnosis of Alzheimer's dementia that includes both Medicaid and Medicare claims data, researchers found significant differences in costs of care by race / ethnicity. 576 These results demonstrate that Black / African Americans had significantly higher costs of care than whites or Hispanics / Latinos, primarily due to more inpatient care and more comorbidities. These differences may be attributable to laterstage diagnosis, which may lead to higher levels of disability while receiving care; delays in accessing timely primary care; lack of care coordination; duplication of services across providers; or inequities in access to care. However, more research is needed to understand the reasons for this health care disparity.
Doctors use several methods and tools to help determine whether a person who has memory problems has possible Alzheimers dementia or probable Alzheimers dementia. Ask person and family member or friend questions about overall health, use of prescription and over - counter medicines, diet, past medical problems, ability to carry out daily activities, and changes in behavior and personality. Conduct tests of memory, problem solving, attention, counting, and language. Carry out standard medical tests, such as blood and urine tests, to identify other possible causes of problem Perform brain scans, such as computed tomography, magnetic resonance imaging, or positron emission tomography, to rule out other possible causes for symptoms. These tests may be repeated to give doctors information about how persons memory and other cognitive functions are changing over time. Alzheimer's Disease can be definitely diagnosed only after death, by linking clinical measures with examination of brain tissue in autopsy. People with memory and thinking concerns should talk to their doctor to find out whether their symptoms are due to Alzheimers or another cause, such as stroke, tumor, Parkinsons Disease, sleep disturbances, side effects of medication, infection, or non - Alzheimers dementia. Some of these conditions may be treatable and possibly reversible. If diagnosis is Alzheimers, beginning treatment early in the disease process may help preserve daily functioning for some time, even though the underlying disease process cannot be stopped or reverse. Early diagnosis also helps families plan for the future. They can take care of financial and legal matters, address potential safety issues, learn about living arrangements, and develop support networks. In addition, early diagnosis gives people greater opportunities to participate in clinical trials that are testing possible new treatments for Alzheimer's Disease or other research studies.
Plex.page is an Online Knowledge, where all the summaries are written by a machine. We aim to collect all the knowledge the World Wide Web has to offer.
© All rights reserved
2021 made by Algoritmi Vision Inc.
If you believe that any of the summaries on our website lead to misinformation, don't hesitate to contact us. We will immediately review it and remove the summaries if necessary.
If your domain is listed as one of the sources on any summary, you can consider participating in the "Online Knowledge" program, if you want to proceed, please follow these instructions to apply.
However, if you still want us to remove all links leading to your domain from Plex.page and never use your website as a source, please follow these instructions.