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 https://www.mundewadiayurvedicclinic.com and http://www.ayurvedaphysician.com
