Alzheimer’s disease is “an irreversible, progressive brain disease that slowly destroys memory and thinking skills, eventually even the ability to carry out the simplest tasks” according to the Alzheimer’s Association. Alzheimer’s affects mostly senior citizens, and symptoms first appear in most people between 60 and 70. The first signs of Alzheimer’s, though, can be noticed between the ages of 30 and 65. However, it is very rare for younger people to exhibit symptoms. Most cases of dementia are caused by Alzheimer’s disease [1]. It is known that all Alzheimer’s patients have dementia; however, one cannot say that all dementia patients have Alzheimer’s disease. Alzheimer’s is a deadly disease, finishing predictably in death [2].

Alzheimer’s disease is named after Dr. Alois Alzheimer. In the early twentieth century (1906), Dr. Alzheimer observed alterations in the brain tissue of a woman who had expired of an uncommon mental disease. Her signs involved loss of memory, language difficulties, and erratic conduct. After her death, Dr. Alzheimer inspected her brain and discovered many uncharacteristic clusters (now called amyloid plaques) and scrambled packets of filaments (now called neurofibrillary, or tau, tangles) [1].

Based on his findings, he correctly theorized that these anomalous buildups were accountable for the patient’s loss of memory and other mental complications.

The plaques and tangles in the brain are some of the foremost characteristics of Alzheimer’s disease. Another characteristic is the damage of contacts between nerve cells (neurons) in the brain. Neurons conduct communications between different segments of the brain – for example, they conduct communications from the brain to muscles and organs in the body. Many other multifaceted brain alterations are thought to play a function in Alzheimer’s disease.

In the beginning, this impairment seems to take place in the hippocampus of the brain. The hippocampus is the part of the brain that is indispensable in forming memories. When neurons perish, further parts of the brain are distressed. In the last stage of Alzheimer’s, destruction is extensive, and brain tissue has shortened substantially.

How many Americans have Alzheimer’s disease?

It is estimated   that more than 5 million Americans may have Alzheimer’s disease. If existing population developments continue, the number of people with AD will increase significantly. However, this trend can be stopped if the disease can be effectively treated or prevented.

The reasons people develop Alzheimer’s are still not fully understood. One known reason is aging.   Age is the most significant accepted risk factor for Alzheimer’s disease. In 2010, in the United States, close to 5 million people 65 years and older were living with Alzheimer’s illness. A 2013 report from the Alzheimer’s Association suggests that 1/10^th of all Americans over 65 are suffering from Alzheimer’s. The proportion goes up to about a third of the population for those who are over 85. According to the Alzheimer’s Association, AD incidence is between 60% and 80% of all incidents of dementia [3].

Incidence of Alzheimer’s disease in South Asia

Globally, at least 44 million individuals live with dementia, making the disease a worldwide health catastrophe that must be tackled. In excess of 4 million individuals have some appearance of dementia in India [4].

In the Southern Indian state of Kerala, 1066 qualified members who were cognitively regular at reference, 104 of them acquired dementia (98 of them were found to have AD) over a continuation time of 8.1 years. The occurrence rates per 1000 person-years for AD was 11.67 for persons aged ≥55 years and greater for those aged ≥65 years (15.54). Individuals who were aged ≥65 years, the global age consistent occurrence rate, was 9.19 per 1000 person-years, prevalence rate of AD raised substantially and proportionally with growing age. These are the initial AD occurrence rates to be conveyed from southern India. When compared to reports from rural North India these occurrence rates appear to be much greater. But they are comparable with those reported from China, and slightly lesser than that reported from the western world [5].

Signs of Alzheimer’s disease

Memory difficulties are characteristically one of the first signs of Alzheimer’s; nonetheless, early indications may differ from individual to individual. A decrease in other facets of thinking, for example forgetting words, sight/three-dimensional problems, and diminished thinking or decision making, may additionally indicate the precise initial periods of Alzheimer’s disease. Mild cognitive impairment (MCI) is a disorder that can be an initial mark of Alzheimer’s. However, not everyone with MCI will develop Alzheimer’s.

Patients with Alzheimer’s have difficulty performing routine things like paying bills, driving a car, or cooking food. They repeatedly ask the same questions, go astray without difficulty, misplace things or put them in unusual places, and find even easy things puzzling. As the disease advances, some patients become anxious, wrathful, or furious.

Longevity of a person with Alzheimer’s disease?

At the time of diagnosis, if the person is older than 80, they are only likely to live another three or four years. If the person is younger then 80, they could live for as many as ten years or more.

Currently Alzheimer’s disease is graded as the sixth greatest cause of death in the United States. But fresh evaluations show that the illness may be listed as third, after heart disease and cancer, as a source of death for elderly people.

At the present time, there is no cure for Alzheimer’s. However, treatment can help patients cope with symptoms [1].

In the 21^st century, Alzheimer’s can only be diagnosed with 100 percent precision through a postmortem examination that discloses the occurrence of the distinctive plaques and tangles. However, a complete examination and suitable checkup can afford a dependable diagnosis with better than 90 percent certainty.

Malformed accumulations of particular proteins inside the brain interrupt normal brain performance and produce the reasoning and efficient difficulties characteristically connected with Alzheimer’s Disease. Ultimately, as the sediments expand all over the brain, brain material begins to die. This results in additional intellectual damage. CT scans and MRI scans show the subsequent brain contraction. CT scan shows enlargement of the ventricles in the brain and loss of brain tissue in a patient with Alzheimer’s disease. Recent research is endeavoring to ascertain what produces these accumulations and is watching for techniques to avoid or change them before they cause lasting brain destruction [2].

Alzheimer’s is not curable.
Alzheimer’s is not contagious.
Alzheimer’s is not a natural part of the aging process.
Alzheimer’s is not something you get from using deodorant or cooking in aluminum pans.
Alzheimer’s is not inevitable if you live long enough.

In some families, Alzheimer’s disease is hereditary. But these appearances are very rare, and they account for fewer than five percent of all incidents. If a family member like a mother or a brother has Alzheimer’s disease, it doesn’t inevitably mean that you’re prone to contract it as well.

There is no test that can foretell whether you’ll get Alzheimer’s disease, save tests for the very rare hereditary Alzheimer’s. A blood test can tell whether you have a certain form of cholesterol-carrying protein connected with an elevated occurrence of the disease. This examination can’t convey whether you’ll actually contract the condition; at least 50 percent of people who have an elevated risk factor never get Alzheimer’s.

Taking into consideration medical ethics, healthcare authorities counsel against taking this blood test or undertaking other genetic testing because they want to save their patients from unwarranted fear about something that will perhaps never happen. There are others reasons for which they also advise against testing. If a person has the inherited gene or elevated risk factor, it might negatively affect their ability to acquire health insurance or long-term care.

Causes of AD

All types of dementia are a result of brain cell death. As such, Alzheimer’s Disease is also caused by brain cell death. When there is an ongoing brain cell death occurring over a period of time, then it is called a neurodegenerative disease. When the brain tissue has an increasingly smaller number of nerve cells and connections, then the total brain size shrinks due to Alzheimer’s.

Plaques in the brain are a result of the build-up of a protein called beta-amyloid (also known as “amyloid plaques”). These plaques cannot be seen or tested for in the living brain affected by Alzheimer’s Disease. A postmortem or autopsy will show these plaques and masses. Plaques are found between the dying cells in the brain.

These unusual protein clusters in the brain tissue are always present with Alzheimer’s disease. Scientists are not yet sure if there could be an additional primary activity that is really causing Alzheimer’s Disease. This sort of alteration in brain nerves is also observed in other illnesses. Researchers want to find out how these protein abnormalities progress so that a cure or treatment might be discovered. Researchers have not completely comprehended why the alterations that lead to Alzheimer’s disease befall a patient. It is known that several dissimilar factors are believed to be implicated, aging and a family history of Alzheimer’s, chief among them.

Diagnosis

Alzheimer’s disease is not straightforward to diagnose, as there is no single test for it. The first step physicians take is to rule out other complications before validating whether mental indications and signs are stark enough to be a type of dementia or something else.

Signs and symptoms [6]

Phases of Alzheimer’s Disease:

Aging has effects on memory but not AD.

• Occasionally forgetting things.
• Sometimes items are misplaced.
• Slight temporary memory loss.
• Not recalling precise particulars.

Early phase

• Not recollecting incidences of deprived memory.
• Forgetting names of family or friends.
• Only close friends or relatives may notice the changes.
• Some perplexity in conditions outside the acquainted.

Middle-phase

• Enormous effort recollecting newly acquired knowledge
• Increasing misperception in numerous situations
• Difficulties with slumber or sleep
• Difficulty in recognizing where they are

Late-phase

• Low capability to reason
• Difficulties in talking
• Retelling same dialogues
• Extra rude, nervous, or suspicious

Treatment

For Alzheimer’s there is no recognized treatment. The loss of brain cells cannot be stopped or overturned.

Drug therapy

There are no disease-altering medicines obtainable for Alzheimer’s, but some choices may decrease its symptoms and help recover quality of life. Four drugs are available. They’re called cholinesterase inhibitors. They include Donepezil (brand name Aricept), Rivastigmine (Exelon), and Tacrine (Cognex). Another type of drug, called memantine (Namenda), which is an NMDA receptor antagonist, may also be used. This drug may be used alone or with a cholinesterase inhibitor.

Other therapies

As with other kinds of dementia and neurodegenerative illness, a chief part of therapy for patients with Alzheimer’s comes from the patronage given by healthcare personnel. Quality-of-life care becomes more imperative as needs increase with diminishing freedom [3].

There are other treatments outside the US. In India, Alzheimer’s disease is treated with Ayurveda [7]. Ashwaganda, an ancient Herb used in Ayurveda, is confirmed to be a possible cure for Alzheimer’s [8]. It has also been found that Curcumin (in India it is called Haldi) is more efficient at hindering the formation of the protein fragments than many other potential Alzheimer’s treatments. Optimizing vitamin D and vitamin B12 intake, as well as a nutritious diet rich in folate and coconut oil, have also been tested as to their efficacy at treating Alzheimer’s Disease [9].

Daily mental challenges

Mental stimulation, particularly acquiring something novel, such as learning to play an instrument or a new language, is linked with a reduced risk of Alzheimer’s. Researchers theorize that mental tasks assist in developing the brain, making it less prone to the lesions connected with Alzheimer’s Disease [8].

References

1. What Is Alzheimer’s Disease? National Institute on Aging, U.S. Department of Health and Human Services. https://www.nia.nih.gov/health/what-alzheimers-disease
2. Alzheimer’s for Dummies, Patricia B. Smith, Mary M. Kenan, Mark Edwin Kunik, Leeza Gibbons. October 2003. http://www.dummies.com/health/knowing-what-alzheimers-is-and-is-not/

3. What’s to know about Alzheimer’s disease? Medical News Today. Newsletter. 13 February 2018. https://www.medicalnewstoday.com/articles/159442.php
4. About Alzheimer’s and Dementia. org. India, Alzheimer’s association. https://www.alz.org/in/dementia-alzheimers-en.asp
5. Incidence of Alzheimer’s disease in India: a 10-years follow-up study. Mathuranath PS1, George A, Ranjith N, Justus S, Kumar MS, Menon R, Sarma PS, Verghese J. Neurol India. 2012 Nov-Dec;60(6):625-30 https://www.ncbi.nlm.nih.gov/pubmed/23287326

6. Alzheimer’s disease. From Wikipedia, the free encyclopedia. https://en.wikipedia.org/wiki/Alzheimer%27s_disease
7. Treating Alzheimer’s disease with the help of Ayurveda by Hunila. November 1, 2012 org. http://www.alzheimerindia.org/treating-alzheimers-disease-with-the-help-of-ayurveda/

8. Ashwaganda: Ancient Herb Proven to be a Potential Cure for Alzheimer’s by Dr. Mercola April 07, 2012 https://articles.mercola.com/sites/articles/archive/2012/04/07/ashwaganda-effect-on-alzheimers-disease.aspx

9. Coconut Oil and Alzheimer’s Disease By anh-usa (Alliance for Natural Health) on October 5, 2010. http://www.anh-usa.org/coconut-oil-and-alzheimers-disease/

The miracle of life appears in the form of a baby which develops from a fertilized ovule (zygote) following millions of other events. This series of events, which is almost always the same for every fetus, can be grouped as reproduction, differentiation, and development. The zygote completes its development in the womb; postnatal growth can continue until 20 years of age. Even though every event during the baby’s development seems to take place with chaotic reactions, harmony and order are there for us to discover. One of these astonishing events is the perfectly symmetric growth of the fetus/baby. Most organs in the human body appear in pairs and are symmetric. Babies are born with 300 bones; however, some bones later fuse with other bones, leaving only 208 bones in the adult human. It is still a mystery how long bones such as the humerus, radius, ulna, femur, and tibia are able to grow on both sides of the human body in a symmetrical manner.

Mechanisms that control growth in organs

In vertebrates, both internal developmental programs and the external factors which stimulate or inhibit growth play a role in the ultimate size of an organ. But the relative effects of these two mechanisms can vary significantly in different organs. When pieces of spleen from an embryo that is at a later stage of growth are transplanted to a newly developing embryo, each new piece grows, but not to the size of the original spleen. The total weight of all the transplanted spleen pieces is equal to a normal spleen’s weight. When the spleen reaches a certain weight, growth inhibiting factors are secreted, which stimulate negative feedback mechanisms that limit growth. When a spleen reaches a certain size, the density of the inhibiting factors increases simultaneously, halting growth. Growth in the liver is controlled by extracellular factors (various substances in the blood, hormones, vitamins, minerals, etc.). When a section is cut off of the liver, the section continues growing and developing until it reaches the size of the original liver. The thymus has a growth process that is executed by a cellular genetic program. When sections of a thymus taken from the embryonic period are injected into developing mouse embryos, every section grows until it reaches the ultimate size.

More evidence of cellular growth programs was acquired via an experiment that was carried out with the salamander genus Ambystoma. When the leg bud of the larger species was injected into the smaller species, it would at first grow slowly, but then it would reach the normal size of its own species (the larger species).

Distinguishing growth and symmetry from one another

Both the arms and legs have long bones. A long bone consists of two parts (diaphysis and epiphysis). The diaphysis is the middle (core) part of the long bone. It consists of hard bone tissue, and is like a tube. The hyaline cartilage-covered joint forms the epiphysis of the long bone. In a growing bone, there is a growth plate (epiphysis plaque) made of hyaline cartilage; this is located between the diaphysis and the epiphysis. The epiphysis plaque causes the bone to grow longer; when growth is complete, the epiphysis plaque ossifies (becomes bone). In other words, growth stops. There are some clues that show the existence of positive feedback mechanisms which control the symmetric and balanced development of the arms and legs while the fetus is still growing. The arms and legs grow due to the development and growth of the plaques located at opposite ends of the long bone. The ultimate size of the arms and legs are proportional to the size of the finger bones (phalanx) and the metacarpus. According to current knowledge, growth in our arms and legs is only controlled by internal growth programs and the active growth of the plaques. We do not yet know the mechanism through which how much the bone must grow and symmetrically with the organ (the other arm or leg) on the other side of the body. But even if this is discovered in the future, we will continue to appreciate the perfect and miraculous aspect of this phenomenon.

In addition, in growth-plaque transplant experiments, the development of the transplanted growth plaque is dependent only on the age and size of the donor. Growth plaques cause the bone to grow, but the plaques themselves remain the same size for years. The cartilage cells they produce (chondrocytes) exchange places with the bone cells (osteocytes) in harmony and without destroying the length of the bone. Cells from different areas of the growth plaque act differently. Stem cells are found on the upper section, near the epiphysis. Immediately above them is an area where cells reproduce very quickly. At the bottom of the epiphysis, the cartilage cells grow up to 4 to 10 times larger than their normal size (hypertrophy). Cell reproduction here is mostly due to hypertrophic chondrocytes. The chondrocytes die and break up, then change places with the bone tissue. The dynamic process of these events in the growth plaque repels it from the bone area, and as a result, the bone grows longer.

Sustained symmetry despite cell sequence and speed of reproduction

The rapid growth rate in the legs and arms during the embryonic period continues to increase until the child is three years of age. This growth rate slows down until the individual reaches adolescence. During the fastest growth period, which is from adolescence to the early 20s, the growth rate rapidly increases. For example, most people who grow between 30 and 37.5 cm during the first two years of life can grow between another 7.5 and 10 cm every year during adolescence. At the onset of adolescence, rapid growth due to a sudden change in the volume of cells is observed. After adolescence a sudden falling off in the speed of growth can be observed due to the effect of hormones on the growth plaques in the spine and other long bones. The growth plaque now fuses with the neighboring cells and growth stops. However, the fusing of the growth plaque is the result of the cessation of growth, not the cause. After growth stops, the growth plaques begin to disappear. When the reproduction potential of the cartilage cells in the growth plaque has been exhausted, the growth plaque begins to disappear.

Growth plaques in different bones can trigger growth at various rates; these rates can differ as much as seven times. In fact, growth plaques on different ends of a bone can have different growth rates, provided that this rate is consistent with the genetic program. The number of cells on the growth line is 40 times more than in other areas. The number of cells produced here can exceed 10,000 cells per day. For symmetric growth between the arms and legs to be sustained, the number of cells in the growth plaque must be the same or very close. Experiments carried out on rats show that eight cartilage cells leave the growth plaque to exchange places with cells above them every day. It can be said that the growth of the bone is caused by the increase of cells in the growth plaque (which sustains its size). The growth rate caused by the growth plaque can be calculated by multiplying the growth plaque’s cell production rate by the average length of all of its cells. Different growth plaques provide different growth rates. This difference can be caused by the difference in the size of the growth plaques, the difference in cell production rates, and/or the difference in the hypertrophy (growth) rate of every cell. The upper growth plaque in the tibia of mice generates 16,400 cells every day; the average life span of these cells is around 30 hours. Can such harmonious, symmetric, and equivalent growth in the arms and legs-despite the large number and variety of cells-be the work of pure coincidence, mindless nature, or unconscious molecules?

Do hormones play a role?

The main molecular players that organize longitudinal growth in bones during childhood are the growth hormone, the thyroid hormone, and corticoids. The sex hormones (androgens and estrogens) are programmed to influence growth during adolescence. Estrogen is the main determiner of characteristics related to increased height and an increase in bone quality, as well as adolescent-related physiology. These hormones are in charge of coordinating growth throughout the body. It is for this reason for women, after the menopause, the production in estrogen decreases and osteoporosis and brittle bones can occur. According to the current view, cartilage cells have a certain genetic reproduction potential, and when this potential finishes, growth stops. The growth rate during the embryonic period is 20 times higher than that of mid-childhood. The growth rate drops greatly during mid-childhood. If we exclude the noticeable increase during adolescence, the cells responsible for growth have begun to age. The bones on opposite sides of the body stay about the same size, despite all of these changes in growth rates. Circulating hormones and neuroendocrinal factors are believed to play important roles in maintaining symmetric growth. But there is no conclusive evidence to support this belief. Even though one can think of factors such as pressure, tension, and sports as helping control harmonious and symmetric growth of bones, no proof has been attained from controlled experiments. As a person ages, a gradual decrease in growth can be observed. Even if a growth plaque is placed into another organism, be it young or old, the growth rate of the bone does not change. This shows that symmetric growth in long bones is controlled by a program that is operated by internal factors, which is also compatible with the genetic program. When chemical-based medication is given to postpone growth, after the medication has been eliminated, the growth plaques grow faster for a short period to compensate for the lost time. These findings show that timing and the location and circumstances of the cell are critical parameters for reproduction. If the cartilage stem cells in the growth plaque have a certain reproduction potential, then it is clear that cartilage cell reproduction stops when growth comes to an end. If growth inhibiting factors slowly accumulate in the growth plaque, this might cause a deceleration of growth over time. Another possibility is some sort of “meter” in the unconscious and mindless stem cells, which keeps track of the number of cell divisions and thus controls aging. The estrogen in our body has a duty of closing down the growth plaques and speeding up the aging of cells. However, we should not forget that estrogen plays the special role of closing down all of the growth plaques at the same time. Estrogen is one of the visible causes of fertility, growth and development, and resilience. Estrogen also represents femininity and fertility at all levels.

When the signals from unconscious cells in the growth plaques and the quite sophisticated interactions among all the factors that influence growth, all of which require an all-encompassing knowledge to be executed, are taken into account, the impeccable genetic programs of different growth plaques on the two sides of the body that leads to the formation of the arms and legs, as if they have been molded in a factory, is absolutely amazing for anyone who reflects upon it.

References

• Wolpert L. (2010).”Unsolved Mystery: Arms and the Man: The Problem of Symmetric Growth.” PLoS Biology. 2010 Vol. 8(9). pp 1-3
• Extremity Development during the Embryonic Period (www.visembryo.com)