Are all dementia a symptom of Alzheimer’s disease? #MentalHealthAwareness
Memoon Zehra, Farooq Ali Khan , Abhishek Kumar, Raamesh Gowri Raghavan and Sukant Khurana
Alzheimer’s disease is a chronic neurodegenerative pathology and most common form of senile dementia which could usually occur in patients over 60 years of age [Early onset of AD was quite rarely reported (1–5%)]. It accounts for almost 70% of all dementias. It is characterized by a decline in memory, language, problem-saving and other cognitive skills that affect a person’s ability to perform every day task.
This decline occurs because neurons in parts of brain involved in cognitive functions have been damaged or destroyed. In Alzheimer’s disease the damage and destruction of neurons eventually affects other parts of brain, including those that affect other parts in the brain such as walking and swallowing. People in final stages are often bed-bound and require around-the-clock care. Alzheimer’s disease is ultimately fatal.
Based on its age of onset, AD is classified into:
Early onset AD — before the age of 65 (1–5% of all the cases.)
Late onset AD– after the age of 65 (95–99% of all the cases.)
Although there are no significant difference in the clinical symptoms of the two types of the disease, its considered that the early onset AD is connected with faster progression and different inheritance patterns.
Symptoms of Alzheimer’s disease
Memory loss that disrupts daily life.
Challenges in planning or solving problems.
Difficulty completing familiar tasks at home, at work or at leisure.
Confusion with time and place
Difficulty in judgment, decision making and reasoning.
Pathology of Alzheimer’s disease
Several mechanisms are involved in AD pathology, such as the presence of neurofibrillary tangles, inflammation processes, and neuronal degeneration. Nevertheless, one of the major characteristics of Alzheimer’s disease is the presence of senile plaques in brain regions. These plaques are formed by a dense core of aggregated amyloid-peptide.
This peptide is formed by photolytic process of by the action of beta secretase and gamma secretase amyloid precursor protein (APP). Furthermore, many studies have demonstrated the relationship between Alzheimer’s Disease and neuroinflammation, which may be a consequence of a systemic inflammatory process that occurs throughout life.
Brain changes associated with Alzheimer’s disease
The accumulation of the protein BETA-AMYLOID outside the neurons and the accumulation of an abnormal form of protein, TAU-TANGLES inside neurons are two of the several brain changes believed to contribute to the damage and destruction of neurons that result in memory loss and other symptoms of Alzheimer’s disease.
The accumulation of BETA AMYLOID interferes with the neuron to neuron communication at synapses and to contribute to cell death.
TAU TANGLES block the transfer of nutrients and other essential molecules inside neurons and are also believed to contribute to cell death.
The brains of people with advanced Alzheimer’s disease show inflammation, dramatic sinkage from cell loss and widespread debris from dead and dying neurons.
Genetic abnormalities that cause Alzheimer’s disease
GENETIC MUTATIONS (1%) : Individuals with mutation of AMYLOID PRECURSOR PROTEIN (APP) and PERNISILIN 1 are guaranteed to develop Alzheimer’s .Those inheriting PERNISILIN 2 gene have 95% chances.
DOWN SYNDROME : People with down syndrome have additional copy of chromosome 21, which includes a gene that encodes for the production of APP, which in people with Alzheimer’s is cut into beta-amyloid fragments that go on to accumulate into the hallmark amyloid plaques of Alzheimer’s.
Risk factors for Alzheimer’s disease
AGE : Age and likelihood of Alzheimer increases simultaneously.it is greatest risk factor, Though, Alzheimer is not a normal part of aging. only old age alone is not sufficient to cause this disease.
FAMILY BACKGROUND : When disease run in famlies, heredity (genetics), shared environmental and lifestyle factors, or both may play a role. The fact of incresed risk because of family history is not entirely explained by whether th eperson has inherited the APOE-e4 gene.The person having first degree relative with Alzheimer’s Disease is at high risk, and those having more than one are at even higher risk.
APOE-e4 (APOLIPOPROTEIN) : 40–60% people diagnosed with Alzheimer had e4. Though, inheriting e4 form of APOE gene doesn’t guarantee the disease. the APOE gene provide the blueprint for a protein that tansports cholestrol in the blood stream. everyone inherits one of the three genes; e2, e3 and e4. RISK- e4> e3> e2.
Modifiable risk factors
CARDIOVASCULAR DISEASE RISK FACTOR : Health of brain is closely linked to health of heart and blood vessels, due to need of getting supply of oxygen and nutrient rich blood to function normally. Thus, cardiovascular diseases could affect brain and lead to increased risk of dementia. Physical activity, healthy diet with low saturated fats can help reducing Alzheimer and dementia’s risk.
EDUCATION : According to COGNITIVE RESERVE HYPOTHESIS , having more years of education increases connectivity between neurons and enable brain to compensate for the early changes of Alzheimer by using alternate routes of neuron-to-neuron communication to complete a cognitive task.
SOCIAL AND COGNITIVE ENGAGEMENT : Remaining socially and mentally active throughout life may help building a cognitive reserve, but the exact mechanism by which this may occur is unknown.
TRAUMATIC BRAIN INJURY ( TBI) : Individuals who have experienced repeated TBIs are at higher risk of dementia, cognitive impairment and neurodegenerative disease than those who haven’t experienced. RISK- severe TBI> 4.5 moderate TBI> 2 no TBI.
Treatment of Alzheimer’s disease
NON PHARMALOGIC TREATMENT : These are often used with goal of maintaining and improving cognitive functions, the ability to perform activities of daily living, or overall living of life. They also focus on reducing behavioral symptoms such as depression, apathy, wandering, sleep disturbance, agitation and aggression.
PHARMALOGIC TREATMENT : No such pharmalogic treatment is available today for Alzheimer which slows or stops the damage and destruction of neuron that causes Alzheimer’s symptoms and make disease fatal.
Although current medications can’t cure Alzheimer or stop it from progressing, they may help lessening symptoms such as memory loss and confusion, for a limited time, by increasing amount of chemicals called neurotransmitters in brain. Some approved medications are:
NAME
Donepezil
Galantamin
Memantive
Rivastigmine
Memantive-donepezil
BRAND
Aricept
Razadyne
Namenda
Exelon
Namzaric
APPROVED FOR
All stages
Mid to moderate stage
Moderate to severe
Mild to moderate
Moderate to severe
Common Side effects of medicines of Alzheimer’s disease
Nausea
Vomiting
Dizziness
Loss of appetite
Increased frequency of bowel movements
bruising
Factors contributing to the difficulty of effective treatments
High cost of drug development.
Relatively long time needed to observe whether an investigational treatment affects disease progression.
Structure of brain, which is protected by the blood-brain barrier through which only very specialized small-molecule drugs can cross.
New approach for treatment of Alzheimer’s Disease
In decades of research, scientists have focused on eliminating the signature plaques of Alzheimer to fight the devastating disease. Now, a drug in phase- 2 trials is taking a new approach, focusing on strengthening cell’s protection against neurological attacks, which may be a game changer.
Population impacted by the disease
According to ALZHEIMERS DISEASE INTERNATIONAL, almost 36 million worldwide suffer from dementia and the number is expected to increase more than triple by the mid of century.
In India more than 4 million people have Alzheimer and similar dementias.
In Asia alone nearly 61 million people will be affected by 2050.
In China more people will suffer from dementia than in all industrialized countries put together.
In Europe the number of cases will nearly double from around 10 million to just fewer than 19 million.
Some 15 million of those affected will be living in the European Union.
In Germany the no of cases are expected to rise from around 1.3 million today to 2.6 million.
Is dementia disease of industrialized countries and western world only?
Recent studies have concluded that prevalence of Alzheimer’s disease has been underestimated, and was long suspected that it is a disease of industrialized countries and western world only. This was due to fact that in many countries had relatively low life expectancy, so that the no. of people who reached the age of 60 or over ( who constitutes the main risk group) was significantly smaller than in the industrialized world and thus has kept the no. of cases down.
Moreover, most countries lack diagnostic means. In many developing countries it is regarded as normal for elderly people to become little bit “odd”.
Difference apparently also exists with regard to life style factors.
Cost of Alzheimer
World Alzheimer’s Report 2015 showed that the then annual cost of dementia is Us $818 billion, and it was expected to become a trillion dollar disease by 2018. More than 70% patients are usually cared by at home. According to Swiss Collection, in advanced stages the cost can be as high as 93000 euros even if person affected lives at home. However according to Vienna Regional Health Insurance, the cost of formal care is much higher.
Living with Alzheimer’s disease
Despite of lack of disease-modifying therapies, studies showed that active management of Alzheimer and other dementias can improve quality of life through all stages of the disease for individuals with dementia and their active management includes:
Appropriate use of available treatment options.
Effective management of co-existing conditions.
Coordination of care among physicians, other health care professionals and lay caregivers.
Participation in adult day care programs and activities.
Taking part in support groups and supportive services.
Organizations raising money for Alzheimer’s research
Alzheimer’s drug discovery foundation.
The Alzheimer’s foundation of America.
Alzheimer’s research program.
Banner Alzheimer’s initiative.
Coins for Alzheimer’s research.
Cure Alzheimer’s fund.
Alzheimer’s society (UK)
Research centers studying Alzheimer’s prevention and causes of Alzheimer
University of California-Irvine, AD research center.
Washington University at St. Louis, AD research center.
University of Washington Alzheimer’s Research Centre.
Emory University Alzheimer’s disease center.
University of Texas, Southwestern Medical center.
REFRENCES:
v World Alzheimer’s report 2016
v World Alzheimer’s report 2015
v International statistical classification of diseases and related health problems, 10th
v Revision. Geneva, World Health Organization, 1992.
v World Alzheimer’s Report 2009. London, Alzheimer’s disease International, 2009.
v Research Article; Selenofuranoside Ameliorates Memory Loss in Alzheimer-Like Sporadic Dementia: AChE Activity, Oxidative
Stress and Inflammation Involvement
v 2016 facts and figures of Alzheimer’s dementia
v Alzheimer’s Association (2011): Alzheimer’s Association report. 2011 Alzheimer’s disease.
v Allianz demographic pulse- www.allianz.com
v Biomedical research international
v Fox news
Alzheimers
About:
Dr. Sukant Khurana runs an academic research lab and several tech companies. He is also a known artist, author, and speaker. You can learn more about Sukant at www.brainnart.com or www.dataisnotjustdata.com and if you wish to work on biomedical research, neuroscience, sustainable development, artificial intelligence or data science projects for public good, you can contact him at skgroup.iiserk@gmail.com or by reaching out to him on linkedin https://www.linkedin.com/in/sukant-khurana-755a2343/.