Diagnosis And Treatment Of Alzheimer’s Disease

What Is The Outlook For People With Alzheimers Disease

Alzheimers disease gets worse over time and is ultimately fatal. Persons with Alzheimers disease live, on average, four to eight years after diagnosis. Some patients can live as long as 20 years after diagnosis. The course of the disease varies from person to person.

Last reviewed by a Cleveland Clinic medical professional on 03/18/2019.

References

How Common Is Alzheimers Disease

Alzheimers disease is the most common cause of dementia . Alzheimers disease is the sixth leading cause of death in the United States.

One in 10 people older than 65 and nearly half of people older than 85 have Alzheimers disease. Alzheimers disease can also affect people in their 40s. The percentage of people who have Alzheimers disease rises every decade beyond the age of 60. According to the Alzheimer’s Association, with the aging of the population and without successful treatment, there will be 14 million Americans and 106 million people worldwide with Alzheimers disease by 2050.

Challenges Of Nanoparticle Technologies

A number of studies have demonstrated promising results for the potential treatment and management of AD using nanocarriers. However, the translation of this technology into the clinic has been slow and sparse. The discrepancy between in vitro and in vivo results, as well as regulatory barriers, have been significant challenges in advancing nanomedicine beyond the benchtop. Nanotoxicity is a major concern in clinical trials and is dependent on multiple factors ranging from formulation to dosage to cell type. One reason for the discrepant results might be attributed to the adsorption of specific proteins onto the surface of nanoparticles . Upon entrance into a physiological environment, the nanoparticle immediately attracts various proteins and biomolecules to its large surface area, known as the protein corona. The formation of the protein corona can determine the cytotoxicity, bioavailability, and effectiveness of these nanoparticles, which poses a major hurdle in their translation.

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Alternatives To Targeting A

In recent years, there have been an increasing number of clinical trials targeting the microtubule-associated protein, tau . Tau is an essential component of the neuronal cytoskeleton, involved with intracellular trafficking and stabilization of microtubules . Tau pathology is found in a range of neurological diseases, including progressive supranuclear palsy, traumatic brain injury, stroke, frontotemporal lobe dementia, Picks disease, and AD . Moreover, in AD, Tau and A dysfunction are inextricably linked, with evidence showing tau as an effector downstream of A other studies demonstrate a feedback loop relationship . Recent drug targets focused on tau are aimed at regulating post-translational modifications, such as hyperphosphorylation, acetylation and glycosylation, as well as aggregation . These post-translational modifications of tau can improve clearance and inhibit tau accumulation , e.g., using phosphodiesterase inhibitors . Furthermore, methods to directly reduce tau expression using small interfering RNA or antisense oligonucleotides as well as the synthesis of active and passive antibodies against tau are being pursued .

Getting An Alzheimer’s Disease Diagnosis At Bwh

An Alzheimer’s disease diagnosis begins with comprehensive evaluations that may include:

• Neurological exams to determine what physical capabilities might be impacted.
• Mental state exams to assess cognitive abilities like memory, language, attention, reasoning, and visual/spatial functioning. This exam may also look at psychological issues around mood and behavior.
• Neuropsychological and neuropsychiatric assessments depending on the patient’s history and initial evaluation, a neurologist may refer the patient to other team members for more comprehensive cognitive testing.
• Brain imaging to identify conditions like strokes or tumors that may be affecting memory. Brain imaging can also detect brain atrophy or shrinkage, and a PET scan may be used to help distinguish an Alzheimer’s disease diagnosis from diagnosis of other neurodegenerative conditions.
• Blood tests may be used to help rule out brain dysfunction due to metabolic and endocrine disorders or infectious diseases.
• Spinal fluid tests to measure abnormal proteins in the spinal fluid that are associated with Alzheimer’s disease and to rule out infection or inflammation.

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Plasma Biomarkers Of Ad

Other approaches using genomics, transcriptomics, metabolomics, lipidomics, and proteomics have been used to generate different AD biomarkers. One study showed that altered microRNAs resulting from the failure of synaptic function are potential plasma biomarkers of AD.5959. Siedlecki-Wullich D, Català-Solsona J, Fábregas C, Hernández I, Clarimon J, Lleó A, et al. Altered microRNAs related to synaptic function as potential plasma biomarkers for Alzheimer’s disease. Alzheimers Res Ther. 2019 11:46. Another study comparing AD patients with healthy controls showed decreased platelet levels of one member of the a disintegrin and metalloproteinase family: ADAM10, the primary -secretase of APP, which plays an important role in reducing generation of A peptide. The same study showed decreased presenilin levels in platelets and leukocytes. Presenilin is the catalytic site of -secretase, one enzyme in the reaction that generates A peptide. Levels of the -site APP-cleaving enzyme 1 , also known as -secretase, were also decreased in leukocytes and presented no differences in platelets.6060. Bram JM, Talib LL, Joaquim HP, Sarno TA, Gattaz WF, Forlenza OV. Protein levels of ADAM10, BACE1, and PSEN1 in platelets and leukocytes of Alzheimer’s disease patients. Eur Arch Psychiatry Clin Neurosci. 2019 269:963-72.

How Is Alzheimers Disease Diagnosed

These tests are used to diagnose Alzheimers disease or to rule out other medical conditions that cause symptoms similar to Alzheimers disease:

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Psychological And Psychosocial Therapies

Psychological therapies for dementia include some limited evidence for reminiscence therapy , some benefit for cognitive reframing for caretakers, unclear evidence for validation therapy and tentative evidence for mental exercises, such as cognitive stimulation programs for people with mild to moderate dementia. Offering personally tailored activities may help reduce challenging behavior and may improve quality of life. It is not clear if personally tailored activities have an impact on affect or improve for the quality of life for the caregiver.

Adult daycare centers as well as special care units in nursing homes often provide specialized care for dementia patients. Daycare centers offer supervision, recreation, meals, and limited health care to participants, as well as providing respite for caregivers. In addition, home care can provide one-to-one support and care in the home allowing for more individualized attention that is needed as the disorder progresses. Psychiatric nurses can make a distinctive contribution to people’s mental health.

Some London hospitals found that using color, designs, pictures and lights helped people with dementia adjust to being at the hospital. These adjustments to the layout of the dementia wings at these hospitals helped patients by preventing confusion.

Cognitive training

Personally tailored activities

Biomarkers For Earlier Detection

Biomarkers are one of the newest potential tell-tale signs of early Alzheimers disease. Research is ongoing on this technology and method of detection. Some biomarkers being studied include beta-amyloid and tau levels. Beta-amyloid deposits of protein fragments are known to build up in between nerve cells. Tau, another protein, resembles twisted fibers that build up inside cells. It is the damage and subsequent death of nerve cells that cause memory failure and other aspects of the disease.

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Emotion And Behavior Treatments

The emotional and behavioral changes linked with Alzheimers disease can be challenging to manage. People may increasingly experience irritability, anxiety, depression, restlessness, sleep problems, and other difficulties.

Treating the underlying causes of these changes can be helpful. Some may be side effects of medications, discomfort from other medical conditions, or problems with hearing or vision.

Identifying what triggered these behaviors and avoiding or changing these things can help people deal with the changes. Triggers may include changing environments, new caregivers, or being asked to bathe or change clothes.

It is often possible to change the environment to resolve obstacles and boost the persons comfort, security, and peace of mind.

The Alzheimers Association offer a list of helpful coping tips for caregivers.

In some cases, a doctor may recommend medications for these symptoms, such as:

• antidepressants, for low mood

develops due to the death of brain cells. It is a neurodegenerative condition, which means that the brain cell death happens over time.

In a person with Alzheimers, the brain tissue has fewer and fewer nerve cells and connections, and tiny deposits, known as plaques and tangles, build up on the nerve tissue.

Plaques develop between the dying brain cells. They are made from a protein known as beta-amyloid. The tangles, meanwhile, occur within the nerve cells. They are made from another protein, called tau.

What Causes Alzheimers Disease

Alzheimers disease is caused by the abnormal build-up of proteins in the brain. The build-up of these proteins called amyloid protein and tau protein leads to cell death.

The human brain contains over 100 billion nerve cells as well as other cells. The nerve cells work together to fulfill all the communications needed to perform such functions as thinking, learning, remembering, and planning. Scientists believe that amyloid protein builds up in the brain cells, forming larger masses called plaques. Twisted fibers of another protein called tau form into tangles. These plaques and tangles block the communication between nerve cells, which prevents them from carrying out their processes. The slow and ongoing death of the nerve cells, starting in one area of the brain then spreading to other areas, results in the symptoms seen in patients with Alzheimers disease.

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Can Alzheimer’s Disease Be Prevented

As the exact cause of Alzheimer’s disease is not clear, there’s no known way to prevent the condition.

But there are things you can do that may reduce your risk or delay the onset of dementia, such as:

• staying physically fit and mentally active

These measures have other health benefits, such as lowering your risk of cardiovascular disease and improving your overall mental health.

Read more about preventing Alzheimer’s disease.

Medication For Alzheimers Disease

As it progresses, Alzheimers damages and destroys brain cells called neurons. These cells are the brains messengers. Medications cant stop the damage, but they can slow some symptoms by improving communication among neurons.

Mild to moderate Alzheimers disease: Medications called cholinesterase inhibitors can control symptoms related to thinking and behavior. These medications provide acetylcholine, a chemical messenger that becomes depleted as Alzheimers progresses. They include:

Moderate to severe Alzheimers disease: A drug called memantine supports brain functions such as memory, attention and language in later stages of Alzheimer’s. It also can make it easier to do daily activities.

Other medications approved by the U.S. Food and Drug Administration for moderate to severe Alzheimers include:

• Rivastigmine as a patch
• Memantine and donepezil

Managing mental health: Depending on your symptoms and health, we may prescribe medications for mood and behavior. These symptoms include depression, anxiety, aggression and sleeplessness. Managing symptoms helps make the patient more comfortable, and supports the caregiver.

We may prescribe medicines such as:

Some sleep, anti-anxiety or antipsychotic medications may be dangerous for people with Alzheimers disease. Check with your doctor before taking any new medications.

Learn more about medications for Alzheimers from the National Institute on Aging.

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Nanocarriers As Diagnostic Tools In Ad

One of the main problems of AD is its late diagnosis due to the delayed manifestation of first clinical symptoms compared to the onset of its molecular and cellular manifestation in the brain. When the first symptoms appear, the neuronal damage is already established and irreversible. Therefore, devices that can recognize AD biomarkers in the early stages preceding memory loss and cognitive decline have attracted much interest in clinical research. Historically, the first clinical biomarker of AD was the A peptide of senile plaques, which accumulates in the gray matter of AD brains. Thus, nanodevices specific for A have been designed for diagnostic purposes .

Another diagnostic application of nanocarriers is the specific binding of disease-specific proteins. As explained above, CFS and plasma show some of the molecular alterations that occur in the brain parenchyma of AD patients, with levels of A peptides, tau, NfL, and SNAP-25, among others, increased in both. Nanocarriers could act as uptake tools to monitor these biomarkers, thus contributing to a solid diagnosis of the stage and severity of AD pathogenesis .

Treatment For Moderate To Severe Alzheimers

A medication known as memantine, an N-methyl D-aspartate antagonist, is prescribed to treat moderate to severe Alzheimers disease. This drugs main effect is to decrease symptoms, which could enable some people to maintain certain daily functions a little longer than they would without the medication. For example, memantine may help a person in the later stages of the disease maintain his or her ability to use the bathroom independently for several more months, a benefit for both the person with Alzheimer’s and caregivers.

Memantine is believed to work by regulating glutamate, an important brain chemical. When produced in excessive amounts, glutamate may lead to brain cell death. Because NMDA antagonists work differently from cholinesterase inhibitors, the two types of drugs can be prescribed in combination.

The FDA has also approved donepezil, the rivastigmine patch, and a combination medication of memantine and donepezil for the treatment of moderate to severe Alzheimers.

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Early Diagnosis And Treatment Of Alzheimers Disease

Recently, focus on early detection, diagnosis and treatment of Alzheimers disease has been increasing. The rationale is that, as with any other serious illness, early intervention will lead to better outcomes for patients and families. Despite the intuitive appeal of this rationale, there is discussion and even debate regarding the issues surrounding early detection and treatment. This review begins with a futuristic case that is aimed at focusing this discussion/debate and then proceeds to consider each of the issues including: should AD screening be part of routine physical examinations? is the amyloid hypothesis correct?: implications for diagnosis and treatment? can neuroimaging studies be used to detect brain amyloid? can symptomatic medications be combined to facilitate cognition? can cognitive rehabilitation programs facilitate cognition? and can immunotherapy and other plaque-busting therapies modify the progression of AD?

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Treatment For Mild To Moderate Alzheimers

Treating the symptoms of Alzheimers can provide people with comfort, dignity, and independence for a longer period of time and can encourage and assist their caregivers as well. Galantamine, rivastigmine, and donepezil are cholinesterase inhibitors that are prescribed for mild to moderate Alzheimers symptoms. These drugs may help reduce or control some cognitive and behavioral symptoms.

Scientists do not yet fully understand how cholinesterase inhibitors work to treat Alzheimers disease, but research indicates that they prevent the breakdown of acetylcholine, a brain chemical believed to be important for memory and thinking. As Alzheimers progresses, the brain produces less and less acetylcholine, so these medicines may eventually lose their effect. Because cholinesterase inhibitors work in a similar way, switching from one to another may not produce significantly different results, but a person living with Alzheimers may respond better to one drug versus another.

Before prescribing aducanumab, doctors may require PET scans or an analysis of cerebrospinal fluid to evaluate whether amyloid deposits are present in the brain. This can help doctors make an accurate diagnosis of Alzheimers before prescribing the medication. Once a person is on aducanumab, their doctor or specialist may require routine MRIs to monitor for side effects such as brain swelling or bleeding in the brain.

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Menieres Disease Home Treatments

Itâs not clear you can do anything to prevent Meniereâs disease, but you can do a few things to help manage your symptoms.

If youâre having an attack of vertigo:

• Try to sit down and stay still.

• Donât make sudden movements, and avoid bright light, loud noise, and other triggers. Watching TV or even reading also can be harmful.

• Fix your gaze on something steady.

In addition to eating a low-salt diet, you may want to cut down on alcohol and caffeine. Some people think such diet changes lessen the effects of the disease. Tobacco use also can be harmful, as cigarettes have chemicals in them that restrict blood vessels. If this happens in your ears, it can lead to hearing loss. Studies show that smokers are much more likely to have hearing loss than nonsmokers.

Vertigo attacks can be triggered by different things in different people. Try to write down as many things as you can remember about the episode. Triggers might include:

• Sharp changes in weather, specifically air pressure

• Underlying illness

Conventional Ad Biomarkers In Csf/plasma

A-related biomarkers

In AD pathogenesis, the production of A peptides is increased, while their clearance is reduced. A1-40 and A1-42 fragments predominantly form, promoting the aggregation of these peptides and thus leading to the formation of senile plaques . A42 is one of the most toxic isoforms of the A peptide and is also one of the most widely accepted biomarkers of AD diagnosis . A42 quantification in CSF allows the identification of AD in its preclinical stage, and possesses high diagnostic value with clear specificity for AD over other neurodegenerative diseases. However, absolute A42 levels vary due to a variety of factors, particularly interindividual differences . To account for these, the ratio between A42/A40 is also commonly used. A40 concentration is 10-times higher than A42 in CSF and its level does not usually vary in AD . Similarly, the A42/A38 ratio is emerging as a potential predictive tool with comparable power to the A42/A40 ratio .

BACE1, the key enzyme that initiates the formation of A peptide , has increasingly been studied as a potential AD biomarker. BACE1 can be measured in CSF, but there is controversy regarding its predictive value. Some studies have shown increased levels and protein activity of BACE1 in AD patients and that this is a good predictor of the progression of MCI patients . However, more recent studies have reported no changes in CSF BACE1 levels among controls, MCI and AD patients .

Tau-related biomarkers

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