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By Dr. Md. Shahjalal Chowdhury, BUMS (DU), MPH (Epidemiology) Lecturer, Community Medicine, Hakim Said Eastern Medical College & Hospital, 37, Nimtoly, Dhaka & Health Program, Talker Bangladesh Betar. Email: dr.jalalshorna.bd@gmail.com

Title: Elderly Alzheimer Disease & Unani Medicine

Introduction: Alzheimer’s disease (AD) is a brain disorder named after German physician Aloes Alzheimer, who first described it in 1906. Alzheimer’s disease is a progressive and neurodegenerative disease & it is the most common cause of dementia in worldwide affects over 44.6 million people, Already 62% of people with dementia live in developing countries, but by 2050 this will be rise to 71%. The prevalence has been found to rise exponentially with age, ranging from 3.0% in patients aged 65 to 74 years to as much as 47.2% in those aged 85 years but It’s primarily affects the elderly population of over 65 years of age. The most common form of dementia is AD, which demolishes the vital brain cells, causing trouble with memory, thinking, and behavior, brutal enough to affect work, lifelong hobbies, and social life. The loss of memory is considered to be the result of a shortage of the nerve transmitter acetylcholine. It is possible to increase the level of this transmitter in the brain by inhibiting the activity of the enzyme acetylcholinesterase, which splits or breaks down the transmitter substance. Drugs that inhibit the breakdown of the messenger or transmitter acetylcholine delay the development of the disease. Alzheimer’s is the most common form of dementia

Causal & Risk Factors: In order to stimulate the innate ability of the body to heal the causes of disease must be identified and addressed. In the case of Alzheimer's disease the causes are variable and include lifestyle and environmental factors. A detailed assessment is required to determine which factors are contributing to the development and progression of Alzheimer's disease.

Lifestyle Dietary factors •	Diets high in saturated fatty acids and trans fatty acids may increase aluminum induced damage to neurons. •	Nutritional deficiencies, especially deficiencies in B vitamins, especially Vitamin B12, iron, zinc, calcium or omega-3 fatty acids can increase the risk of Alzheimer's disease. •	Diets high in sugars, both glucose and fructose, contribute to Alzheimer's disease Exercise •	Regular physical exercise, including aerobic conditioning, is beneficial and been shown to decrease the likelihood of developing Alzheimer's. •	Cognitive exercises including crossword puzzles, music, art, and headline discussion can help to preserve cognitive function. Just as physical exercise is important in preventing dementia and Alzheimer’s, cognitive exercise is protective against cognitive decline. Interestingly, AD risk declines based on years of formal education, further suggesting that cognitive stimulation decreases risk of Alzheimer's disease. •	Sleep: There is an integral relationship between sleep, circadian rhythm physiology and Alzheimer's disease. Disorders in sleep or circadian disturbances can lead to AD and in turn AD leads to disorders in sleep and circadian disruption Social Stress: Studies have shown that increased stress has significant impacts on development and progression of cognitive decline. Stress causes the release of cortisol which has been shown to inhibit learning and memory. Techniques used to reduce stress, such as meditation, have been shown to positively benefit cognitive function in AD patients. Economic Status:  It has been suggested that the correlation between education level and AD risk factor may actually represent socioeconomic status or early childhood medical and psychosocial environment. Environmental Time Spent Outside: There is evidence that decreased exposure to sunlight in early mornings may increase risk of AD. Heavy Metals: Aluminum: During the 1960s and 1970s, aluminum emerged as a possible suspect in causing Alzheimer’s disease. This suspicion led to concerns about everyday exposure to aluminum through sources such as cooking pots, foil, beverage cans, antacids, and antiperspirants. Since then, studies have failed to confirm any role for aluminum in causing Alzheimer’s, but few experts believe that continuous exposure to aluminum source may cause threat. There is some post-mortem evidence of increased aluminum levels in AD sufferers. The neurofibrillary tangles considered a hallmark of AD contain up to four times the normal level of aluminum compared to brain tissue in unaffected individuals. It is postulated that aluminum interferes with transport and synthesis of acetylcholine, and the production of dopamine, norepinephrine, and serotonin. External Accidents: Brain injury in early life doubles the risk of AD development; moderate head injury triples the risk of AD, whereas serious, severe head injury quadrupled AD risk. Genetics: AD has a strong genetic component - there are several known genes associated with AD. The gene for the amyloid precursor protein occurs on chromosome 21 which explains the link between Down's syndrome and AD. Like many chronic disease, while genetic components are important, lifestyle & environmental factors remain crucial in determining AD risk. According to a growing body of evidence, risk factors for vascular disease ― including diabetes, long term high blood pressure, Heart Disease and high cholesterol, Older age the risk of getting AD doubles every 5 years after 65, History  of Head trauma, Downs syndrome and stroke-related dementia. Common Symptoms: The symptoms associated with Alzheimer's disease includes: 	Progressive mental deterioration 	Loss of memory and cognitive functions 	Inability to carry out activities of daily life (ADLs) 	Anterograde amnesia typically presents first and most intensely 	Apathy and loss of initiatives 	Paranoia 	Delusional thinking 	Irritability

Diagnosis: A diagnosis of Alzheimer's disease is one of exclusion, and can be made after ruling out other possible causes of dementia. •	Assessment and monitoring of AD can be performed using mini-mental status examinations. •	There are no laboratory tests available to confirm a diagnosis of AD. Some MRI and PET findings may suggest a diagnosis but are not specific or sensitive and are not routinely used. •	Genetic Test: Using a blood test for the APOE-e4 gene. Having the gene may suggest Alzheimer Disease, but it does not always mean someone has the disease. The criteria is based on the DSM-IV include the following: •	The course of AD is gradual with continuing cognitive decline •	The deficits do not occur only during the course of a delirium. •	The deficits are not better accounted for by another disorder such as depression or schizophrenia. Related Symptoms & Conditions •	Dementia with Lewy bodies presents similarly to AD, and suggest the presence of Parkinsonism, hallucinations, and sleep disorders. This correlation between AD and Lewy bodies suggests overlap between the diseases.[5] •	Mild cognitive impairment is a risk factor for developing dementia, and dementia sufferers have a high rate of transition to AD. Mild cognitive impairment is characterized by impairment of episodic declarative memory with normal cognitive function and no substantial interference with work, ADLs, or social activities. Characteristics: It is now clear that changes in the brain occur 30 to 40 years before the onset of dementia and AD. Information from PET scans has demonstrated lesions in individuals' brains long before they are symptomatic. The main lesions implicated in AD are known as plaques and tangles. A protein called beta amyloid is found in abundance in AD patients, and forms plaques on the outside of brain cells. These plaques initiate an immune response which ultimately leads to the death of neurons. Tangles are formed by the Tau molecule, which structurally supports neurons. When this molecule changes shape it causes tangles which also eventually causes neuronal cell death. Oxidative Stress. There is also evidence that increased free radical damage may increase risk of AD.. Usul-e- Ilaz (Method of Unani Treatment): 1.	Treatment according to underlying cause of Disease. 2.	Medication with Dwae-e- Mufferah ( Herbs of Refrigerants) 3.	Medication with Dwae-e- Mukbbi-e-e Dimagh ( Brain Tonic Herbs) 4.	Medication with Muhallel-e-Waram (Anti-inflammatory Herbs) Alzheimer's disease is a chronic disease and requires consistent and comprehensive treatment in order to delay its progression & Goals in treating Alzheimer disease are to also manage behavior problems, confusion & agitation, Provide safe living environment, Support family members & others caregivers. Ilaaz (Unani Treatment): A number of scientific researchers have been carried out on medicinal herbs. Herbs have anti inflammatory and antioxidant activities that may be used in the treatment of AD. Alzheimer’s patients have an acetylcholine deficiency. Anti-inflammatory herbs may reduce inflammation of the brain tissue in Alzheimer’s: German chamomile, Ginseng, licorice, turmeric, and white willow bark. Acetylcholine is a neurotransmitter that plays a key role in cognitive function and reasoning. The brains of those with mild-to-moderate Alzheimer’s disease, a progressive type of dementia, have abnormally low acetylcholine concentrations. This means that any compound that enhances the cholinergic system in the brain may be useful in treating Alzheimer’s disease and similar brain malfunctions. The herbs that inhibit Acetylcholinesterase (AchE) contain natural COX-2 inhibitors, also reported as medicinal herbs, for AD indication.

Some Unani herbs like Guduchi, Padma (Nelumbo nucifera), Shankhpushpi, Pancha-Tikta-Ghruta Gugguli, Amalaki, Musta Arjun, Ashwagandha, Galo Satva, and others are excellent herbs for slowing down the brain cell degeneration caused by Alzheimer’s. They enhance the brain’s ability to function, and therefore, provide stability when used consistently

Dwae-e- Mufferah ( Herbs of Refrigerants): Apple (Malus sylvestri):

Fig: Apple (Malus sylvestri) Prevents neuro-degeneration. Stimulates the brain through increased circulation and oxygenation. .

Cinnamon:

Fig: Cinnamon & Honey

According to Unani Pharmacology Cinnamon is an Exhilarant for mental health that essential for AD. Cinnamon is also effective in preventing or delaying the symptoms of AD. A 2009 study published in the Journal of Alzheimer’s Disease found that an aqueous extract of Ceylon cinnamon helped inhibit tau aggregation and filament formation, two hallmarks of Alzheimer’s disease. Cinnamon and honey are good for relieving nervous tension and improving memory. Research indicates that simply smelling cinnamon can help enhance memory and cognitive function. Plus, it is believed that eating honey at night before going to sleep helps prevent nocturnal metabolic stress. It also promotes sleep, which plays a critical role in the consolidation of memory. Cinnamon also facilitates better blood flow to the brain as well as improved memory and recognition. Additionally, it helps control blood sugar levels in people with diabetes, one of the risk factors for Alzheimer’s. •	Put cinnamon in your tea, toast, cereal, oatmeal, baked goods, fruit salad and smoothies. •	You can also take cinnamon in supplement form. Always consult a doctor for the correct dosage. •	Mix a pinch of cinnamon in about one teaspoon of raw honey. •	Consume this mixture daily at night for at least a few months. Note: Do not take cinnamon in excess as it may be toxic to the liver.