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Friday, November 25, 2016

Can Alzheimer's Disease be Cured?

Alzheimer’s disease is a progressive irreversible neurodegenerative disease of the brain which 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).

Current treatment option for Alzheimer’s include drugs which increase the acetylcholine level in the brain and decrease the neuronal excitotoxicity. Family support or nursing care is vital in the treatment and it is essential that the caregiver knows about the disease and can adequately care for the person with Alzheimer’s disease.

The main goal of 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 no approved treatment is available which targets the disease pathology which means at present there is no cure for the disease. However, scientists are constantly on the lookout for new drugs which can affect the disease pathology, possibly reversing it or curing the patient. But why couldn’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. Entorhinal cortex plays a vital role in 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 disease. As the disease progress further more areas of the brain gets damaged and ultimately this leads to global neurological dysfunction.

    Difference between Alzheimer's brain and normal brain
    Difference between Alzheimer's brain and normal brain

    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 on the pathology of the disease that we have postulated based on current information and research. In 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 types: Late onset 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 onset Alzheimer’s disease 

    This is the most common type of Alzheimer’s disease. We still have not figured out the exact cause behind it but scientists have managed to develop 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 and lifestyle factors.

    Scientists have so far identified one possible genetic variation which if present does increase the possibility and risk of a person developing Late onset Alzheimer’s disease - the Apolipoprotein E (APOE) gene which is located on the chromosome 19.

    The APOE gene is responsible for the production of a type protein called Apolipoprotein E. This protein is one 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 is 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 APOE protein cause Alzheimer’s disease? 
    One of the major ways Alzheimer’s disease develops is by the deposition of Amyloid proteins which are abnormal proteins in the nerve cell which ultimately cause destruction of the nerve cells. The deposition of amyloid plaques in the brain is one of the characteristic findings in Alzheimer’s disease. 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 of age 30 to 60 years and represents around 5% of all Alzheimer’s cases. In majority of the cases, 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 chromosome that are changed are chromosome 1, 14 and 21. Specific inherited defects in any one of these three chromosome leads 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 leads 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 develops Alzheimer’s as they age around 65 years. Down’s syndrome people have an extra copy of chromosome 21. Scientist are still researching on the link between Down’s syndrome and Alzheimer’s disease but one possible explanation is that the presence of an extra copy of chromosome 21 which produces amyloid precursor protein 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 which 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 impairment of memory and learning.

    3. Amyloid protein deposition in 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 in details regarding Tau proteins and how they lead to the Alzheimer’s disease.

    What are Tau proteins? 

    Tau proteins are important structural proteins of microtubules. Microtubules are important components of any 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 disease?

    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. 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 

    Infographic showing the causes of Alzheimer's disease
    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 couldn’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 compared to Alzheimer’s.


    Can genetic tests predict Alzheimer’s disease?

    There are some genetic tests available that can predict the chances of development of Alzheimer’s in a person who is related by birth to someone (positive family history) suffering from the disease. Such test 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 cancer where genetic testing in a person with a positive family history allows that person to take some preventive measures like surgery or chemo-prevention.

    We know more about Alzheimer’s today than we ever did. Even though we can not cure Alzheimer’s disease as of today, we can treat it and minimize the progression and symptoms temporarily and hopefully one day we will finally be able to cure the disease. We will talk more about the latest researches on Alzheimer's disease in the upcoming posts.

    That's all for today!
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