How Is Alzheimers Diagnosed And Treated
Doctors may ask questions about health, conduct cognitive tests, and carry out standard medical tests to determine whether to diagnose a person with Alzheimers disease. If a doctor thinks a person may have Alzheimers, they may refer the person to a specialist, such as a neurologist, for further assessment. Specialists may conduct additional tests, such as brain scans or lab tests of spinal fluid, to help make a diagnosis. These tests measure signs of the disease, such as changes in brain size or levels of certain proteins.
There is currently no cure for Alzheimers, though there are several medicines approved by the U.S. Food and Drug Administration that can help manage some symptoms of the disease along with coping strategies to manage behavioral symptoms. In 2021, FDA provided accelerated approval for a new medication, aducanumab, that targets the protein beta-amyloid, which accumulates abnormally in the brains of people with Alzheimers. The new medication helps to reduce amyloid deposits, but has not yet been shown to affect clinical symptoms or outcomes, such as progression of cognitive decline or dementia.
Most medicines work best for people in the early or middle stages of Alzheimers. Researchers are exploring other drug therapies and nondrug interventions to delay or prevent the disease as well as treat its symptoms.
Pathology Of Alzheimers Disease
Macroscopic features
Fig. 1
Gross Anatomy of Alzheimers Brain. Lateral view of an Alzheimers brain can show widening of sulcal spaces and narrowing of gyri compared to a normal brain. This may be more readily observed in coronal sections as indicated by the arrowheads, and this atrophy is often accompanied by enlargement of the frontal and temporal horns of the lateral ventricles as highlighted by the arrows. Additionally, loss of pigmented neurons in the locus coeruleus is commonly observed in the pontine tegmentum as shown with the open circle. None of these features is exclusive to Alzheimers disease
Microscopic features
The definitive diagnosis of AD requires microscopic examination of multiple brain regions employing staining methods that can detect Alzheimer type neuropathologic change , with diagnosis based upon the morphology and density of lesions and their topographic distribution. Several of the brain regions that are vulnerable to Alzheimer type pathologic change are also vulnerable to other disease processes, such as -synucleinopathy and TDP-43 proteinopathy. Mixed pathology is common. Indeed in the Mayo Clinic Brain Bank from 2007 to 2016 , the majority of AD cases had coexisting non-Alzheimer pathologies, and comorbidities increased in frequency with age. Furthermore, when the original clinical diagnoses were examined for cases with pure AD pathology, it is clear that a number of clinical syndromes can masquerade as Alzheimers disease.
Need For Nanotechnology As A Therapeutic Strategy Across The Bbb
There are promising drugs against A toxicity,75 but in order to explore their maximum effect on CNS cells, there is a need of nanocarriers to be employed. Availability of drugs in the CNS is the major issue faced in the field of therapeutics against AD. The main reason is the presence of a fully functional semipermeable BBB, which poses as an obstacle for transmigration of neurotherapeutic molecules across it, into the CNS. The BBB and its selective transport of molecules into the brain oppose efficacious delivery of therapeutic agents. In addition, the BBB also negatively affects drug efficacy and tolerance, because large doses of drugs are needed to reach levels above the minimum effective concentration in the brain. Nanotechnology inclusive of nanoparticulate systems offer an opportunity to overcome such problems and can be used as Trojan-horse systems for transporting active molecules across the BBB , thus reducing toxicity and improving therapeutic efficacy.76,77
The authors report no conflicts of interest in this work.
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Pathology Associated With Increased App Gene Dose Including Neuronal Loss
A number of aspects of AD pathology have been associated with the additional copy of APP in DS mouse models. This includes the aging-dependent loss of BFCN in the medial septal nucleus and norepinephrine neurons of the LC in the Ts65Dn DS mouse model . In the Ts2Cje mouse model, aging-dependent loss of BFCN in the medial septal nucleus also occurs . Some studies have indicated that the loss of ChAT staining from BFCN is caused by a downregulation of the cholinergic marker rather than the death of neurons , thus the pathology may be reversible and not the result of the death of post-mitotic neurons.
Three copies of the App gene are necessary for BFCN and LC neuronal loss in the Ts65Dn mouse . Reducing BACE1 gene dose also rescues MSN-BFCN cell loss in Ts2Cje mice . BACE1 encodes -secretase that cleaves APP to APP-C-terminal fragment- , suggesting that upregulation of CTF- or a related APP fragment may underlie BFCN degeneration in DS mouse models . Other aspects of neurobiology such as neuroinflammation are likely to contribute to the loss of these neurons in DS mouse models as degeneration has also been rescued by treatment with anti-inflammatory agents, including minocycline and anti-oxidants . A recent study demonstrated that aging-dependent reductions in MSN-BFCN cell density in the Ts65Dn can also be rescued by normalizing Dyrk1A gene dose . Thus multiple mechanisms and Hsa21 genes contribute to neuronal loss in DS models.
Yldz Dincer, in, 2019
How Is Alzheimers Disease Treated
Medical management can improve quality of life for individuals living with Alzheimers disease and for their caregivers. There is currently no known cure for Alzheimers disease. Treatment addresses several areas:
- Helping people maintain brain health.
- Managing behavioral symptoms.
- Slowing or delaying symptoms of the disease.
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Cognitive Reserve And Prevention
The quantitative function known as brain reserve has wide ranging biological implications for the pathogenesis of AD. For example, environmental stimuli trigger upregulation of BDNF and neurogenesis,114116) encouraging neural plasticity.116,117) Cognitive and brain reserves, enhance our understanding of the differences in the clinical pathology of the brains of AD patients.114,116) A number of studies have evaluated the association between leisure activities and AD incidence.114) Engagement in intellectual activities or social activities was assessed in a large cohort of elderly New Yorkers who had not been diagnosed with AD individuals engaged in numerous leisure activities had a dramatically reduced risk of developing AD during follow-up evaluation.118,119)
A And Tau Prions Spread Through The Brains Of Ad Patients
Prion protein is a special conformation of a protein encoded by the host, with self-reproduction ability, superior infectivity, tenacious viability, and the ability to remain concealed, even surviving in the normal denaturing environment of the digestive system. Prions can cause a variety of neurodegenerative diseases in humans, including CreutzfeldtJakob disease , GerstmannSträusslerScheinker syndrome , and fatal familial insomnia in humans . These diseases can occur spontaneously or through genetics or infection.
Studies have shown that A spreads through the brain via a pathogenic conformation similar to PrPSc . Brain-derived A and synthetic A from AD patients injected into the brain of transgenic mice showed prion-like appearances , which induced plaque formation and extensive deposition of A. Brain extracts from age-matched patients without AD showed minimal accumulation of A . An autopsy in a few studies also revealed that some patients had a large amount of A deposition in the brain after death, after receiving dura mater transplantation and cadaveric growth hormone, which may mean that A can be transmitted interpersonally through iatrogenic methods. Prion-like A activity participates in the pathogenesis of AD. The formation of prion-like A begins in one or more brain regions and then spreads to other brain regions, reflecting cross-synaptic transmission.
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Animal Models For Diabetes And Alzheimers Disease Research
As mice and rats are the most widely used animals for biomedical research, we will focus on these preclinical animal models for studying metabolic disorders and neurological pathologies. There are many rodent models available for studying type 1 or type 2 diabetes and Alzheimers disease. New, improved animal models are continuously designed to mimic the diseases in people, yet none of them are a perfect analogue for people . Interestingly, several animal models that were originally designed to study diabetes, obesity, and metabolic syndrome have shown a great potential for studies of neurodegeneration and AD . Normally, rodents do not develop diabetes or AD therefore, an induction of the development of pathologies is needed. There are several ways that diabetes and AD animal models are designed. In this review, we present those that are most often used, are designed by transgenic modifications, or induced by a compound, diet, or lesion. Transgenic modifications are often used to generate rodent models that simulate these human diseases. Genes of main interest for modifications are those that are involved in amyloid- and tau development, lipid metabolism , and genes involved in insulin desensitization . However, other approaches for reproducing human diabetes and AD pathology in animals exist as well. Aging-based models develop the pathologies based on either natural aging or accelerated senescence .
Cholinergic Neurotransmission And Alzheimer Disease
The cholinergic system is involved in memory function, and cholinergic deficiency has been implicated in the cognitive decline and behavioral changes of AD. Activity of the synthetic enzyme choline acetyltransferase and the catabolic enzyme acetylcholinesterase are significantly reduced in the cerebral cortex, hippocampus, and amygdala in patients with AD.
The nucleus basalis of Meynert and diagonal band of Broca provide the main cholinergic input to the hippocampus, amygdala, and neocortex, which are lost in patients with AD. Loss of cortical CAT and decline in acetylcholine synthesis in biopsy specimens have been found to correlate with cognitive impairment and reaction-time performance. Because cholinergic dysfunction may contribute to the symptoms of patients with AD, enhancing cholinergic neurotransmission constitutes a rational basis for symptomatic treatment.
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Alzheimers Disease: An Update And Insights Into Pathophysiology
- 1Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria
- 2Centre for Advanced Medical Research and Training, Usmanu Danfodiyo University, Sokoto, Nigeria
- 3Department of Physiology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
- 4Department of Basic Medical Science, Kulliyyah of Medicine, International Islamic University Malaysia, Kuantan, Malaysia
- 5Department of Clinical Pharmacology, Faculty of Medicine, Menoufia University, Shebin El-Kom, Egypt
- 6Neurology Unit, Department of Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Centre, Kuala Lumpur, Malaysia
What Does Alzheimers Disease Look Like
Memory problems are typically one of the first signs of Alzheimers, though initial symptoms may vary from person to person. A decline in other aspects of thinking, such as finding the right words, vision/spatial issues, and impaired reasoning or judgment, may also signal the very early stages of Alzheimers disease. Mild cognitive impairment is a condition that can be an early sign of Alzheimers, but not everyone with MCI will develop the disease.
People with Alzheimers have trouble doing everyday things like driving a car, cooking a meal, or paying bills. They may ask the same questions over and over, get lost easily, lose things or put them in odd places, and find even simple things confusing. As the disease progresses, some people become worried, angry, or violent.
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Combined Effects Of Antidepressants And Antidiabetic Drugs On Diabetes Cognitive Impairment And Mood Disorders
Interestingly, drugs for treating depression and diabetes were found to have a potential for treating conditions other than that of their primary purpose. Their potential often has joint properties, as some antidepressants help treating diabetes, while some antidiabetics are useful for treating cognitive impairment and mood disorders, which can develop in AD.
Preclinical and clinical studies have shown that serotonergic antidepressants help to improve diabetes and diabetic neuropathy. Antidepressants that increase serotonergic impactfor example, fluoxetinepromote the response to insulin . However, no study has yet proposed a mechanism of action for such positive effects of selective serotonin reuptake inhibitors on glucose homeostasis. In contrast, tricyclic antidepressants and similar ones that impact on norepinephrine are known to increase insulin resistance and cause important cardiovascular side effects . Therefore, it is of great importance to consider which class of antidepressant drugs to use due to their different impact on glucose homeostasis.
Animal Models And Behavior
Memory and learning are dependent upon alterations in synaptic transmission within the hippocampus and other areas of the brain. Transgenic animals that over-express A accurately model familial-type AD and may contribute to increased understanding of the pathogenesis of cognitive and memory deficits.5,99) Synaptic function and plasticity have been extensively studied in transgenic APP and APP/PS mice, with a focus on the dentate gyrus and CA1 subfields of the hippocampus. AD transgenic mice show abnormal synaptic transmission and impaired LTP, often well in advance of plaque formation.3,100102) Memory and learning deficits may occur within 3 months in mouse models, suggesting that soluble A contributes to AD pathogenesis.103,104) Alternate studies report later onset of symptoms at more advanced ages, implicating insoluble A plaques.100,104109) The specific structure of A that is responsible for cognitive deficits has been the subject of great debate. Amygdala-dependent learning is strongly inhibited with increasing age in Tg2576 mice models, suggesting that the amygdala is susceptible to A toxcicity.35,110,111)
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The Pathophysiology Of Dementia: What Causes It
Many of us know someone who is experiencing dementia. What can you do to help them? Understanding dementia and its causes is a good step toward being able to provide your loved ones the support they need.
Dementia is commonly misrepresented as being an illness where you lose your memory. However, dementia is a symptom of various conditions and not a disease in itself. There are several ways it can materialize, with each illness affecting the body physiologically in varying ways. This process is known as the pathophysiology and its goal is to explain the changes that happen in the body when a disease is present. This article will outline the pathophysiology of dementia, including some of the most common ailments that lead to it and general treatment advice for the condition.
Chronic alcohol abuse can shrink brain cells in addition to be being highly dangerous and toxic for other body parts and organs such as the liver and the heart.
Whichever one of these illnesses your loved one is going through, remember you are not alone in this struggle. Support is available.
What Treatment Options Are There for Dementia?
Except for Wernicke-Korsakoff syndrome, dementia and its associated diseases are incurable and cannot be reversed. Treatment cannot address the pathophysiology of dementia in the brain however, it is possible to treat its symptoms.
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New Insights Into The Pathogenesis Of Ad
With the prospect of an increasingly aging society, the number of AD patients and sociomedical burdens will increase dramatically. Currently, cholinesterase inhibitors and the NMDA receptor antagonist are the only therapies for AD . However, these can only relieve symptoms and not delay the progress of AD . Moreover, three cholinesterase inhibitors, namely, donepezil, rivastigmine, and galantamine, which are approved by the US Food and Drug Administration, were proven to increase side effects, such as nausea, vomiting, and diarrhea. Although the NMDA receptor antagonist memantine showed good effects on improving cognitive function and behavioral disturbance scores , it causes severe hypotension, leading to fainting, and falls . According to statistics, AD drug development had a high failure rate of 99.6% in the decade between 2002 and 2012 . Based on these above unsatisfactory results, researchers are constantly proposing new pathogenic mechanisms.
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Global Economic Of Ad
The global burden of AD is expected to accelerate from 26.6 million cases in 2006 to 106.8 million by 2050.3 The total assumed worldwide costs of dementia were US$ 604 billion in 2010, equivalent to 1% of the worlds GDP. Low-income countries accounted for just less than 1% of total worldwide costs , middle-income countries for 10% of the costs and high-income countries for 89% of the costs . About 70% of the global costs occurred in just two regions: Western Europe and North America. These discrepancies are accounted for by the much lower cost per person in lower income countries – US$ 868 in low-income countries, US$ 3,109 in lower-middle-income, US$ 6,827 in upper-middle-income, and US$ 32,865 in high-income countries.6 In high-income countries, informal care and formal social care account for the major costs, while the proportionate contribution of direct medical costs is much lower. In low-income and lower-middle-income countries, direct social care costs are minute and informal care costs predominate. Changing population demographics in many LMIC may lead to a decline in the ready availability of extended family members in the coming decades states the 2012 WHO report Dementia: a health priority.
Fmri With Additional Erp Recording In Motion Perception
fMRI is characterized by excellent spatial resolution, but low temporal resolution. Thus, it can only discriminate between events that are separated by several seconds. In contrast, the temporal resolution of ERPs is in the order of milliseconds, which is far superior to that of other neuroimaging methods including fMRI. However, ERPs offer poor spatial resolution compared with fMRI. Based on these characteristics, the combined use of fMRI and ERPs is considered to be an extremely useful technique for evaluating the spatiotemporal functional changes in AD and MCI in detail. In the following section, we summarize the findings of our studies using fMRI and separate ERP measurement during the performance of motion perception tasks in healthy controls and MCI patients .
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Pathophysiology Of Alzheimers Disease
Info: 1184 words Nursing Essay 17th Jun 2020
Introduction of Alzheimers Disease
Alzheimers Disease is named after Dr. Alois Alzheimer, in 1906 when he noticed changes in the brain tissue of a woman who had died of an unusual mental illness . This mental illness was found to consist of amyloid plaques and tangles in the brain to be considered one of the things present in an individuals brain that is a clear sign of the disease makeup. Alzheimer Disease is a brain disease that causes problems with memory, thinking and behavior most closely associated with dementia. 10% of individuals greater than 65 years of age has Alzheimers Disease and this increases 25% more with individuals greater than 85 years . The disease is commonly affecting the senior population. Intervention amongst Alzheimer patients is a great need for supervision and attention. Intervention amongst caregivers and registered nurses must be a top priority amongst the elderly population. In Alzheimers disease, there is a progressive loss of intellectual function that eventually interferes with work, relationships, and personal hygiene . Alzheimers disease affects 5.3 million individuals in the United States with the elderly population continuing to increase. With the continuing increase of Alzheimer Disease affecting the elderly population, intervention and education are greatly needed.
Etiology and Risk Factors
Pathophysiological Process
Clinical Manifestations and Complications