Tag: Alzheimer’s disease

Alzheimer’s disease is a progressive, irreversible degenerative disease of the brain. Most cases of Alzheimer’s disease are sporadic, but 5% are familial (inherited as an autosomal dominant condition).

Unfortunately, at present, there is no cure for Alzheimer’s disease. At present, the main goal of treatment is to focus on managing the disease symptoms, such as memory loss. Current medications may, for some time, reduce the progression of memory loss and also improve the person’s quality of life by inducing cognitive changes.

The treatment programs vary depending on the stage and symptoms he Alzheimer’s disease, the supporting care facilities available, the presence of any concurrent illness, other drugs taken by the person, which may interfere with the Alzheimer’s medication, and the person’s tolerance to the prescribed medicine. Other than pharmaceutical treatment, it is often recommended that the person be given counseling and other therapies. In a nutshell, at present, we just treat the symptoms, and there is currently no cure available for Alzheimer’s disease, which treats the underlying pathology of the disease and prevents its progression. However, Scientists are constantly trying their best to come up with new medicines that attack the disease at its root and not its symptoms. Still, such drugs require further clinical research and trials before they can be approved for regular clinical use.

Important Facts about Alzheimer’s disease

• The most common cause of dementia in the UK is Alzheimer’s disease,  followed by vascular and Lewy body dementia.
• Alzheimer’s disease is the single most common cause of dementia.
• Approximately 10% of all persons over the age of 70 have significant memory loss, and in more than half, the cause is Alzheimer’s disease.
• In Alzheimer’s and Parkinson’s, olfactory loss may be the first clinical sign of the disease.

Before we talk about the treatment of Alzheimer’s disease, it is important that we cover some basic background information, such as the pathophysiology of Alzheimer’s disease, so that we understand the science behind the treatment.

What is Alzheimer’s disease?

It is a neurodegenerative disease of the brain characterized by progressive loss of short-term memory w,, which is followed by general deterioration of cognitive and other neurological functions. It is present in about 17% of people aged over 65 and 40-45% of people who are aged over 95. It is one of the most common and major medical problems of our time.

What are the causes of Alzheimer’s disease? Basic pathophysiology of Alzheimer’s disease?

To understand the basic mechanism of how Alzheimer’s occurs, we need to understand how the brain transmits information from one nerve cell (called a neuron) to another. Exchange of information between two neurons occurs through the exchange of chemical mediators (such as acetylcholine, noradrenaline, serotonin, dopamine, nd others) which are released at the junction where one neuron ends and another neuron begins. This junction is called a Synapse. In Alzheimer’s disease, this process of information transmission is interrupted, and there is eventual damage and destruction of neurons, which ultimately leads to memory loss, behavioral changes, and other features of Alzheimer’s. The number of neurons lost and the location of the brain that is affected are factors that determine the specific type of disorder that develops. Damage to the noradrenergic, serotonergic, and dopaminergic pathways (these pathways release the neurotransmitters noradrenaline, serotonin, and dopamine) leads to behavior and mood disorders, while damage to the cholinergic neurons (which release acetylcholine – a vital neurotransmitter for memory) leads to memory impairment.

Why is memory loss the first symptom in Alzheimer’s disease?

In Alzheimer’s disease, memory impairment is the prominent feature as the cholinergic neurons are affected first. These neurons release the neurotransmitter acetylcholine, which is crucial for the maintenance of intact memory. As the disease progresses in severity, other neuronal pathways are affected, leading to other features of Alzheimer’s disease, such as behavioral and global cognitive damage.

Pathological progression of Alzheimer’s disease in the brain

In Alzheimer’s disease, the pathology starts in the part of the brain called the entorhinal cortex, from there it affects the hippocampus, then the posterior temporal and parietal neocortex, and ultimately causes global degeneration of the entire cerebral cortex. The main function of the entorhinal cortex is related to memory and navigation. Similarly hippocampus serves to move short-term memory to long-term memory and navigation. The temporal lobe is associated with the maintenance of visual memory, language comprehension, and emotional balance. The parietal neocortex is responsible for language processing and the integration of other sensory information. Since these areas of the brain are predominantly and primarily affected in Alzheimer’s disease, the usual presenting features of Alzheimer’s disease are memory loss, aphasia, and disturbance of language. However, it is seen that around 20% of patients with Alzheimer’s disease initially present with non-memory symptoms such as word-finding, organizational, or navigational difficulty. So, in a nutshell, there is diffuse atrophy of the brain with enlargement of the ventricular system.

Molecular pathology of degenerative dementia in Alzheimer’s disease

Microscopically, there are neuritic plaques containing Aβ amyloid, silver-staining neurofibrillary tangles (NFTs) in neuronal cytoplasm, and accumulation of Aβ42 amyloid in arterial walls of cerebral blood vessels. These are all abnormal protein complexes that damage the synapses and ultimately cause neuronal death.

What are the risk factors of Alzheimer’s disease?

• The main risk factor for Alzheimer’s disease is Age. The incidence of Alzheimer’s increases exponentially with Age.
• Family History: A first-degree relative with Alzheimer’s disease results in a doubled lifetime risk of developing Alzheimer’s disease. Family history usually denotes a genetic cause.
• Presence of other genetic disease: Most Down syndrome patients will develop early-onset Alzheimer’s disease.
• Vascular Risk Factors.
• Female gender: This risk factor may be independent of the fact that females have a longer life span.
• Diabetes increases the risk of Alzheimer’s disease threefold.
• Alzheimer’s disease is more common in people with very low educational attainment, but then again, it can affect people of all intellectual levels.
• Environmental factors like aluminum, memercuryand viruses are suspected to have a role in developing Alzheimer’s disease, but there is not enough evidence behind it.
• Head injury: Boxers and Footballers are three times more likely to develop neurodegenerative diseases than normal people.

What are the clinical features and stages of Alzheimer’s disease?

Initially, the symptoms of memory loss may be ignored by the patient and family member as just simple forgetfulness or clumsiness. Eventually, as the disease progresses, normal day-to-day activities such as driving, shopping, and managing finances are affected. The patient may become lost while driving or even walking. As the disease progresses further, the patient becomes unable to do any work, gets easily confused, and starts requiring supervision. Patients may demonstrate difficulty doing tasks that require eye-motor coordination, such as dressing, eating, solving simple puzzles, and copying geometric features. In the late stages, even though some patients retain the ability to walk around, they do not know where they are going. There is marked impairment of judgment, reasoning, and other cognitive abilities. Delusions become a prominent feature. About 10% of Alzheimer’s patients at this stage develop Capgras’ syndrome, where they believe that their caregiver is replaced by an imposter. Signs of agitation and aggression alternate with inactivity and passivity. The patient’s sleep pattern is affected, and nighttime wandering becomes common. Patient becomes dependent on caregiver or family members for the simplest tasks such as eating, dressing, and others.

What are the treatment options for Alzheimer’s disease?

Now that we have covered the basics of Alzheimer’s disease, let’s focus on the management of the disease. The main goal of treatment in Alzheimer’s disease is the long-term control (delaying the progression and improving the quality of life) of neurological and behavioral problems.

Non-pharmacological approach to treat Alzheimer’s disease

The main treatment has to start within the patient’s family or caregiver because without their constant support, patience, and tolerance, patients with Alzheimer’s cannot survive. Family members should focus their energy on activities that are pleasant and not pay much attention to unpleasant activities. It is important to make the patient feel safe through communication and repeated assurance. As the disease progresses, the patient will start exhibiting symptoms such as aggression, confusion, anger, and other symptoms described, each of which needs to be dealt with calmly. Family members must research Alzheimer’s disease so that they become aware of the disease progression and expect the natural course of the disease. Caregivers must be given a break. Caregiver burnout is very common. It may be required to place the patient in a nursing home specialized in caring for patients with neurodegenerative diseases. We have written an article on how to care for loved ones, such as a parent with Alzheimer’s disease, that you might be interested in reading.

Pharmacological treatment options for Alzheimer’s disease

Medications for the treatment of memory symptoms

The FDA currently approves five drugstment of Alzheimer’s disease. They are: Donepezil, rivastigmine, galantamine, memantine, and tacrine. Tacrine is no longer used due to its severe toxic effects on the liver.

How do Anti-cholinesterase drugs work?

Donepezil, Galantamine, and Rivastigmine are CNS cholinesterase inhibitors, which means they inhibit the action of the enzyme cholinesterase whose function is to break down the neurotransmitter acetylcholine. Since cholinesterase is blocked, less acetylcholine is bro ke down, resulting in an increased level of acetylcholine in the brain, which keeps communication between neurons intact. As discussed earlier, in Alzheimer’s disease, there is a deficient status of acetylcholine in the brain, which leads to impaired memory. Anti-cholinesterases delay the breakdown of acetylcholine, increasing levels in the,, leading to memory improvement. These drugs are also used to improve language, tththinkingcision-makingand, and thought processes. Donepezil is the only anti-cholinesterase drug that is approved to be used in the stages of Alzheimer’s disease. It can also be used in combination with memantine. The other two anti-cholinesterase drugs, rivastigmine and galantamine, are used in mild to moderate Alzheimer’s disease. It is usually seen that anti-cholinesterase delays the progression of Alzheimer’s symptoms by 6 to 12 months.

What are the side effects of Anti-cholinesterase drugs used in Alzheimer’s disease?

Donepezil: Decreased appetite, nausea, vomiting, diarrhea, difficulty sleeping, and muscle cramps. Side effects generally improve with time.

Rivastigmine: Rivastigmine can be given orally or via skin patch. Side effects incl as nausea, vomiting, decreased appetite, and weight loss. Nausea and vomiting are less with skin patches. Skin rashes occur due to severe toxicity and can happen with both oral preparations and NSS patches. For skin patches, the patient and caregivers should be aware of the potential warning signs such as severe itching, rrrednessr iformationat on at the site of the patch. If any signs of toxicity occur, the patch (if used) should be immediately taken off, the site should be washed with water prop, and the patient should be taken to the hospital immediately for evaluation by a doctor.

Galantamine: Side effects include nausea, vomiting, and diarrhea. However, just like donepezil, side effects usually decrease with time. Some less common but serious side effects that were noted in some studies include decreased heart rate (bradycardia), atrioventricular block, and syncope.

How do mementine / Nreceptorotor antagonists work?

N-methyl-D-aspartate (N DA)-receptor (Glutamatergic) antagonist: One of the hypotheses behind the pathology of Alzheimer’s disease is neuroexcitotoxicity. Neuroexcitotoxicity is a pathological process where nerve cells are damaged or even destroyed by excitatory neurotransmitters. Memantine works by blocking the overexcited N-methyl-D-aspartate (N  DA) receptor. It is used in moderate to severe disease where cholinesterase drugs are contraindicated or not tolerated by the patient. It can improve memory, logic, critical thinking, language, and attention. It is seen that the combination of memantine and cholinesterase inhibitors is better than either used alone. Since Donepezil is approved for the treatment of all stages, it is often combined with memantine.

What are the side effects of mementine?

Confusion, dizziness, drowsiness, headache, difficulty sleeping, agitation, hallucinations. Less common side effects include vomiting, anxiety, bladder inflammation, and increased libido.

Treatment for behavioral changes

Why do behavioral changes occur in Alzheimer’s patients?
Behavioral changes in Alzheimer’s patients occur mostly due to damaged nerve cells. However, side effects of medications, environmental factfactorsd the presence of simultaneous medical conditions also contribute to the behavioral changes.

What are the behavioral changes in Alzheimer’s disease?

In the initial st, behavioral changes can be expressed by anxiety, depression, and irritability. As the disease progresses further, symptoms may include anger, aggression, agitation, confusion, hallucination, delusions (such as Capgras’ syndromand and e), sleep disturbances.

How to treat the behavioral changes in Alzheimer’s disease?

The main way to tackle behavioral changes is to identify the trigger that causes a certain type of behavior. The main non-pharmacological approach to tackle such situations is to produce an environment where the patient feels calm and safe. As the diseprogressesress, depression becomes a common problem, and it is often difficult to distinguish between true depression and dementia. Some authorities suggest tantidepressantsshould be tried out on a trial basis if depression is suspected.

Anti-psychotics should only be prescribed (for symptoms like hallucination, delusion, aggression, agitation, and others) as a last option because it is seen that there is an increased risk of stroke in Alzheimer’s patients who take anti-psychotic drugs. If prescribed, then the patient should be carefully monitored.

Alzheimer’s disease is one of the major medical problems of our world today. Statistics say that one in nine people aged over 65 years suffers from Alzheimer’s disease. Since our life expectancy is increasing dramatically with the advancement of the health sector, it is estimated that by 2050, someone in the US will develop the disease every 33 seconds, and the number of people with Alzheimer’s disease will rise from 5.2 million to an estimated 13.8 million. However, scientists are continuously working on improving the treatment outcomes and looking at possible cures and preventive measures of the disease. At present, however, there is no cure for the disease, and the main goal of the treatment right now is focused on managing the memory loss symptoms and behavioral changes. You should also read about the causes of beta amyloid plaque formation in Alzheimer’s disease.

Alzheimer’s disease begins with memory loss

Alzheimer’s disease begins with memory loss, specifically the short-term memory, such as forgetting where one kept his or her car keys or missing important events. Memory loss is the most prominent and initial presenting feature because the pathology starts in a part of the brain called the entorhinal cortex, which is responsible for the maintenance of intact memory. As the disease progresses and affects other parts of the brain, other symptoms and signs start to appear. People start forgetting where they are or how they got there. They may get lost while driving or even walking. They have difficulty expressing themselves and show poor judgment. Behavioral changes like aggression, anxiety,  and confusion occur, and they may suffer from depression. A caregiver needs to know how to care for his or her loved ones, such as parents or other close relatives who are suffering from Alzheimer’s disease.

How to take care of a loved one with memory loss due to Alzheimer’s disease?

As discussed above, initially, short-term memory is affected. Unfortunately, as the diseases progress, the long-term memory is also affected, which is called amnesia. It is an extremely important and sensitive topic to discuss because memory is what defines a person. We will discuss this another day about what memory is and how it develops.

Memory loss not only affects the individuals suffering from it but also those supporting them. In the initial stages of memory loss, people are usually aware of the changes that are taking place. Some people get easily frustrated, while some get anxious. Some lose their self-confidence and get embarrassed. Some may even withdraw from social gatherings. One of the most painful things that happens in the later stages is difficulty in recognizing people, including family members.

Let’s discuss a few ways you can help your loved one with Alzheimer’s disease

1. Stay calm. It is extremely important for family members to stay calm and expect the symptoms and signs that come with the natural progression of the disease. As a caregiver, you must analyze and respond to every situation calmly.
2. Try to evoke memory inpositivelyAvoid directly telling your loved one that they had the same conversation before or that they have met with someone particular before. Instead, use pictures or other items that can provoke thoughts that will help the person recall information.
3. If something is not important to remember, then do not force it. Ask yourself whether it is really important for your loved one to remember certain information. If not, do not try to force him or her to recall it. It might lead to unnecessary confusion and agitation.
4. Follow a routine. It is seen that following an established routine in life helps the person remember what is going to happen.
5. Set up an emergency pocket notebook that should include all the essential information in case the person gets lost. This should include the person’s name, address, emergency contact number,  er and other essential details. Instead of a notebook, an ID bracelet could also be used. You could also invest in a locator device that uses GPS to track the person.
6. Help them keep a journal to track the things that have happened and to keep a to-do list.t
7. You can even give them a camera to take photos regularly. The type of camera will obviously depend on the person’s ability to use it properly, but it can be a digital camera, a Polaroid camera, or even a phone. Ask them to associate the photo with the journal. There are even automated cameras out there today that will automatically take around 100 pictures or so at regular intervals in a day.
8. Ask them simple, straightforward questions like “Are you hungry?” instead of “Have you had lunch?”. When you go out to eat, instead of asking them what they would like to eat, it is better to give them a menu or options so that they can choose.
9. If something needs to be explained, then do it simply. Do not use complicated words or expressions, and if necessary, repeat your explanation.
10. If they are struggling to converse, then do not rush them. Instead, pause for a while so that they can find the word. If they are talking for a long time, then offer them suggestions based on the surrounding context. Be patient and do not jump to completing their sentence; instead, help them remember the words.
11. Help them recall someone by introducing them like this:  “Here is your granddaughter, Mom.” This way, the person will not get embarrassed.
12. Avoid places that are too crowded with high background noise. Try to establish a calm, relaxed environment where the person will not feel stressed out. Stress can hamper the memory even more.
13. Set up a particular place to keep regularly used items such as keys or glasses. If necessary, use labels or sticky notes to identify them. Always keep an extra pair of important items, such as keys, glasses, ready. Do not stress them if they can not find something that can be easily replaced. Instead, calm them down and help them remember only if it is necessary. Remember, if it is not important, then do not force it. Fortruly valuable things and a duplicate can not be produced readily, can tagging them with a small tracking system will help you locate them.

Alzheimer’s disease is a progressive and irreversible neurodegenerative disease of the brain that mainly affects people over 65 years of age. It is the number one cause of dementia. It most commonly presents with the symptoms of memory loss (initially short-term memory loss).

The main goal of the current treatment regimen is to slow down the rate of progression of the disease and improve the memory impairment. Although such measures are only temporary, they play a vital role in the quality of life of a person who is suffering from Alzheimer’s disease.

At present, approved treatment is available that targets the disease pathology, ic h means that at present, there is no cure for the disease. However, scientists are constantly on the lookout for new drugs that affect the disease pathology, possibly reversing it or curing the patient. But why can’t we find a cure for Alzheimer’s disease yet? To understand the answer to this question, it is important to have some knowledge about the basic pathology of the disease. Let’s cover some basic background information on Alzheimer’s first.

Which area of the brain is affected first in Alzheimer’s disease?

In the brain, the first area to be affected by Alzheimer’s disease is the entorhinal cortex. The torhinal cortex plays a vital role in the maintenance of a person’s memory and navigational abilities. More specifically, in Alzheimer’s disease, the lateral entorhinal cortex seems to be affected first by Alzheimer’s. As the disease progresses further, more areas of the brain get damaged, and ultimately, this leads to global neurological dysfunction.

How does the brain get damaged in Alzheimer’s disease?

For most cases (95% to 98%), the exact cause is unknown! We can only move forward based on some hypotheses about the disease’s pathology that we have postulated based on current information and research. In the rest of the cases, a genetic defect can be identified, which can be attributed to the development of Alzheimer’s disease.

So, what are the possible causes of Alzheimer’s disease?

1. Genetic defects

Alzheimer’s disease can be broken down into two main typeslate-onsetet Alzheimer’s disease and early-onset Alzheimer’s disease. The late-onset AD is the most common, and it affects people aged over 65. There are genetic components associated with both of these types of Alzheimer’s disease. Late-onsetAlzheimer’s disease

This is the most common type of Alzheimer’s disease. We still have not determined the exact cause, but scientists have developed several solid hypotheses. It is usually said that the cause of this variant of Alzheimer’s disease is multifactorial, which means that this disease develops as a result of the combined effect of a person’s genetics, environmental, nd lifestyle factors.

Scientists have so far identified one possible genetic variation,,,,chif present in, iincreases the possibility and risk of a person developing Late onset Alzheimer’s disease – the Apolipoprotein E (APOEgene, which is located on chromosome 19.

The APOE gene is responsible for the production of a type of protein called Apolipoprotein E. This protein is one of the major transport proteins for cholesterol, fat-soluble vitamins, and other types of fat in the lymphatic system and blood.
There are three main varieties of this protein:

• APOE ε2: This is the least common variant, and the presence of this protein may actually provide some protection against Alzheimer’s disease.
• APOE ε3: This variety is the most common, and the presence of this variety neither increases nor decreases the risk of developing Alzheimer’s disease.
• APOEε4: This variety is associated with an increased risk of developing Alzheimer’s disease.

What is important to remember is that the presence of APOE ε2 or APOE ε3 does not mean that a person will not develop Alzheimer’s disease. Similarly, the presence of APOEε4 does not guarantee the development of Alzheimer’s disease.

How does the APOE protein cause Alzheimer’s disease? 
One of the major ways Alzheimer’s disease develops is by the deposition of Amyloid proteins,  which are abnormalities in the nerve cells that ultimately destroy the nerve cells. The deposition of amyloid plaques in the brain is one of the characteristic findings in Alzheimer’s disease. The APOE protein helps in the breakdown of these abnormal amyloid proteins. However, the APOEε4 variant is less efficient at breaking down these proteins, which makes individuals having the APOEε4 variant more susceptible to developing Alzheimer’s disease.

Early-onset Alzheimer’s disease

This variety of Alzheimer’s disease occurs in people aged 30 to 60 years and represents around 5% of all Alzheimer’s cases. In the majority of cases, a familial inherited change in one of three particular chromosomes leads to the disease, which is called the Early Onset Familial Alzheimer’s disease. The three chromosomes that are changed are chromosomes 1, 14, and 21. Specific inherited defects in any one of these three chromosomes lead to Alzheimer’s disease.
Mutated genes in these three chromosomes are responsible for the production of three different types of proteins:

• Mutated genes in chromosome 1 produce the protein Presenilin 2
• Mutated genes in chromosome 14 produce the protein Presenilin 1
• Mutated genes in chromosome 21 produce the protein Amyloid precursor protein

These mutated genes and the abnormal proteins produced by them ultimately lead to an increased production of abnormal amyloid proteins, which get deposited in the nerve cells, particularly neurons, and ultimately cause Alzheimer’s disease. As discussed in Late Onset Alzheimer’s disease, the deposition of amyloid plaques in the brain is one of the characteristic findings of Alzheimer’s disease.

It is interesting to note here that 50% people with Down’s syndrome eventually develop Alzheimer’s disease at an early age of 40 years. The rest developAlzheimer’s as they age around 65 years. Down syndrome has an extra copy of chromosome 21. Scientists are still researching the link between Down’s syndrome and Alzheimer’s disease, but one possible explanation is that the presence of an extra copy of chromosome 2,1which produces amyloid precursor protein,, i n leads to increased production and deposition of amyloid plaques in the brain, which causes the early onset of Alzheimer’s.

2. Deficiency of acetylcholine

Acetylcholine is a neurotransmitter that is responsible for the maintenance of intact memory and learning. In Alzheimer’s disease, the cholinergic hypothesis states that there is reduced synthesis of acetylcholine, leading to impaired memory and learning.

3. Amyloid protein deposition ithe n the brain

The amyloid hypothesis suggests that the deposition of abnormal amyloid proteins in the brain is the main reason behind the development of the disease. Indeed, the presence of beta amyloid plaques is one of the characteristic findings of Alzheimer’s disease. These beta amyloid proteins are produced in excess (a few possible explanations for the increased production of amyloid proteins have already been discussed above) and damage nerve cells, which ultimately leads to the development of Alzheimer’s disease.

4. Abnormal Tau protein

Tau proteins are normal components of nerve cells, particularly neurons, and Alzheimer’s disease is said to develop when these tau proteins become defective. Indeed, the presence of large numbers of abnormal tau proteins, also known as Neurofibrillary tangles, is the other characteristic finding of Alzheimer’s disease. Let’s discuss TaungTau proteins and how they lead to Alzheimer’s disease.

What are Tau proteins?

Tau proteins are important structural proteins of microtubules. Microtubules are important components of all cells in the body. Tau proteins are mostly found in the neurons, and their main function is to stabilize the microtubules. When tau proteins become defective, they cannot function properly and cannot stabilize the microtubules, which leads to the development of neurodegenerative diseases like Alzheimer’s disease and Parkinson’s disease.

How do tau proteins get defective in Alzheimer’s disease and other neurodegenerative diseases?

The tau hypothesis states that abnormal or excessive phosphorylation of tau proteins causes them to clump together into an insoluble mass of proteins called Neurofibrillary tangles, which are also known as paired helical filaments. The presence of neurofibrillary tangles is one of the main hallmarks of Alzheimer’s disease.

Scientists do not know the exact pathology behind the formation of neurofibrillary tangles, but some causes are:

1. Mutated Tau protein
2. Trauma to the brain
3. Aluminium

Infographic showing the causes of Alzheimer’s disease

Now that we have some basic understanding of Alzheimer’s disease, let’s move on to the next section.

Why can’t we find the cure for Alzheimer’s yet?

The basic problem lies in the fact that Alzheimer’s disease is a multi-factorial disease. It is a combination of genetics, environmental health, and lifestyle choices. To put things into a broader perspective, let’s think about AIDS for a while. Acquired Immune Deficiency Syndrome or AIDS is a disease that is caused by the Human Immunodeficiency Virus or HIV. Even though there is a clear correlation between the disease and the causative factor, we still have not found a cure for AIDS. But since the link between AIDS and HIV is simpler, we have been able to progress much further in terms of knowledge and finding an actual cure for HIV than we have forAlzheimer’s.

Can genetic tests predict Alzheimer’s disease?

There are some genetic tests available that can predict the chances of the development of Alzheimer’s in a person who is related by birth to someone (positive family history) suffering from the disease. Such tests are not recommended for everyone because they are not always accurate. The presence of a genetic risk factor does not mean that the person will always develop the disease (as explained earlier in this article). Moreover, we have no way to prevent the disease, unlike, for example, breast or ovarian can, where genetic testing in a person with a positive family history allows that person to take some preventive measureslike susurgeryr chemoprevention.