Alzheimer disease (AD) is a chronic, progressive, neurodegenerative disorder involving cognitive and behavioral impairment which severely impairs day to day activities, as well as social and occupational functioning. This condition causes dysfunction and atrophy of the hippocampus, a part deep within the brain which helps to encode memories, as well as parts of the cerebral cortex which are involved in thinking and making decisions. Structural changes may begin to appear in the brain several decades before actual appearance of signs and symptoms.
AD usually goes through 4 clinical stages. The first stage is preclinical, in which the hippocampus and nearby brain areas get affected and start shrinking; however, patients are usually clinically unaffected. In the next stage which is termed as mild AD, the cerebral cortex too gets affected, giving rise to symptoms such as memory loss; getting lost; difficulty in doing daily activities, handling finances, making judgments; loss of spontaneity and initiative; and mood and personality changes. The subsequent stage is moderate AD, in which brain parts are involved which control language, reasoning, sensory processing and conscious thought. This causes symptoms such as increased memory loss and confusion; shortened attention span; difficulty with language, learning, logical thinking, recognizing people and organized movement; increased mood and personality changes; and repetitive actions and statements. The last stage is severe AD, in which there is significant atrophy of affected brain parts, because of which patients fail to recognize close or family members; become completely dependent; and lose all communication and sense of self. There may be additional symptoms like weight loss, difficulty in swallowing, incontinence, skin infections, convulsions, and increased sleeping.
Senile plaques (SPs) and neurofibrillary tangles (NFTs) are the hallmark of AD pathology. Plaques are formed by the accumulation of dense, mostly insoluble deposits of a protein known as beta-amyloid (Ab) as well as some cellular material surrounding neurons. Ab is a part of a larger protein known as amyloid precursor protein (APP), which is associated with the neuron cell membrane. Degenerative processes speed up the formation of Ab fragments, which come together outside the cell and form clumps known as SPs. It is currently unclear whether SPs are the cause or byproduct of the AD disease process.
Healthy neurons have an internal communication system partly made up of structures known as microtubules, which allow to and fro movement of nutrients and molecules. A special kind of protein known as tau binds to the microtubules and stabilizes them. AD causes chemical changes in tau which in turn bind together and cause tangling, disintegration and collapse of the microtubular system, leading to disorganized structures known as NFTs. These cause disruption in the communication between neurons, gradually leading to cellular death.
The anatomic pathology of AD thus includes SPs and NFTs at the microscopic level, and cerebro-cortical atrophy at the macroscopic level, which can be visualized in MRI plates. Clinical onset of AD is primarily preceded by accumulation of SPs; while NFTs, loss of neurons and their synaptic connections are associated with progressive cognitive decline. AD thus affects the communication, metabolism and repair of brain cells; progressive neuron cell death causes the clinical features of the disease. The presence of a sufficient number of SPs and NFTs along with a characteristic distribution in the brain is required for a definitive diagnosis of AD, since these may be present in other neurodegenerative diseases, and may also be a part of aging. In addition to SPs and NFTs, other pathological changes may also contribute to the disease process. These include granulovacuolar degeneration (in the hippocampus); formation of neuropil threads (in the brain cortex); cholinergic (neurotransmitter) deficiency; oxidative stress and damage (in the brain); chronic inflammation; clusterin (protein) alterations; increased presenilin (gene) expressions; and estrogen (hormone) loss.
Currently, modern medicine can only offer symptomatic treatment for AD, with most medications modulating neurotransmitters, either acetylcholine, or glutamate. Behavioral symptoms like depression, agitation, aggression, hallucinations, delusions, and sleep disorders can be treated using antidepressants, anxiolytics, antiparkinson medications, beta blockers, antiepileptic drugs and neuroleptics. Graded and interactive mental activities are known to improve cognition and slow down deterioration. Diets which reduce carbohydrate consumption and allow for increased consumption of fruits, vegetables, and non-farmed fish have been known to reverse mild to moderate cognitive decline. Such interventions also include a graded exercise program, stress reduction techniques, and supplementation with vitamin D3, fish oil, coenzyme Q-10, melatonin, and methylcobalamin. Physical activity, exercise, cardiorespiratory fitness, and a Mediterranean diet may have a preventive effect.
In the absence of any specific treatment or cure for AD, Ayurvedic herbal treatment can be utilized judiciously with significant results. AD is treated as a mix of autoimmune and degenerative disorder, and treated using some common treatment principles utilized for such diseases. This includes detoxification, treatment of chronic infection and inflammation, providing specific nutrition for degenerating tissues, opening up of damaged and blocked nutritional pathways, modulating metabolism at the general level as well as cellular level, and repair of reversible damage. These actions are usually performed concurrently, and may need to be tailor-made as per the history, clinical presentation and specific requirements of each individual.
Epigenetics is a change in gene expression that results from gene-environment interactions; this may be brought about by chemical or functional changes in RNA and DNA without actually changing the gene sequence. Epigenetic elements are possible in the causation of AD since the occurrence of AD in the majority of patients is sporadic, without a family history, and presents late in life. Exposure to chemicals, aluminium and lead; chronic oxidative and environmental stress; and chronic inflammation, are known factors which may present using this mechanism. While these are causative factors, the information pertaining to epigenetics can be used in Ayurvedic treatment to reverse the pathology as well as symptoms of AD.
Ayurvedic herbomineral combinations need to be given for several months to reverse AD pathology. The dosage depends upon the severity of symptoms; patients with moderate and severe AD require high doses. These are supplemented with herbs to continue mild detoxification, treat inflammation and provide nutrition. While these medicines are administered orally, there are other treatment modalities also in use. Courses of medicated enemas and medicated nasal drops can bring about significant improvement. A special procedure known as “Shiro-Basti” is used, in which warm Ayurvedic medicated oils are poured onto the scalp within special, elongated skull caps for specific durations. Generalized skin massage and fomentation with medicated steam also provide good results. Exposure to sunlight (known in Ayurvedic terminology as “aatap sevan”) helps AD people to remain active in the day time and sleep well at night. The consumption of various medicated oils, ghee (clarified butter) and bone marrow is also known to provide benefit.
Most of these procedures, as well as oral treatments, require some degree of cooperation from people affected with AD; hence it is advisable to commence Ayurvedic treatment as early as possible, preferably at the time of diagnosis. This can ensure that patients get the maximum possible therapeutic benefit in the form of decreased symptoms, better quality of life, and reduction in morbidity and mortality.
The writer, Dr A A Mundewadi, is available as an Ayurvedic consultant at www.mundewadiayurvedicclinic.com and
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