Neurodegenerative disorders form a group of diseases in which there is a progressive loss of structure or function of neurons or nerve cells in the brain and spinal cord, resulting in progressive degeneration and death of the nerve cells causing problems with movement (ataxia) or with mental functioning (dementia). These disorders are characterized by a standard pathological process involving inflammation; oxidative stress; abnormal depletion or insufficient synthesis of neurotransmitters; and genetic mutations, causing damage to protein synthesis and premature cell death. This results in aggregation or deposit of abnormal protein clumps in various parts of the brain and spinal cord, and characteristic symptoms which help in identifying specific diseases. More than 200 such diseases are listed in this group; the commonly known diseases include Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Amyotrophic Lateral Sclerosis (ALS), and Ataxias [including Spino-Cerebellar Ataxia (SCA)].
AD is characterized by cognitive impairment causing loss of memory; disturbance in reasoning, planning, language and perception; and behavioral changes. This disease causes deposits of fibril clumps of abnormal β amyloid protein known as senile plaques. This causes gross atrophy and degeneration of different parts of the brain including the temporal lobe, parietal lobe, parts of the frontal cortex, and the lingulate gyrus.
PD is a chronic and progressive movement disorder characterized by slow movement (bradykinesia), rigidity, resting tremor, and postural instability. There is an abnormal accumulation of protein known as Lewy bodies, causing death of dopamine generating cells in the substantia nigra, a region of the midbrain. Both AD and PD are usually associated with advanced age.
HD is an adult onset, autosomal dominant, inherited disorder characterized by involuntary movements, dementia, and behavioral changes. There is a loss of neurons in the basal ganglia and frontal and temporal cortex. The subthalamic nuclei send control signals to the globus pallidus which initiates and modulates motion. Weaker signals cause reduced initiation and modulation of movement resulting in the characteristic choreiform (repetitive, rapid and jerky) movements of HD.
ALS is a disease in which motor neurons are selectively targeted for degeneration. Motor neurons are nerve cells located in the brain, brainstem and spinal cord which serve as controlling units and communication links between the nervous system and voluntary muscles of the body. Motor neurons in the brain are known as upper motor neurons while those in the spinal cord are known as lower motor neurons. ALS is a rapidly progressive neurological disease affecting both the upper and lower motor neurons. There is a loss of voluntary control over arms, legs, and respiratory muscles. Muscle wasting, atrophy, and twitching (fasciculation) cause problems with movement, dysphagia (difficulty in swallowing), dysarthria (difficulty in speech) and spasticity. Sensory function and cognition are usually well maintained. ALS pathology includes protein aggregates, mutation in the gene encoding the antioxidant Superoxide Dismutase 1 (SOD 1), and mutation in chromosome 9. The mutation first acts on the local astrocytes, which later causes a toxic effect on the entire motor neuron.
Ataxias are a group of neurological disorders in which there is degeneration and atrophy of the cerebellum, causing abnormal and uncoordinated movements, gait abnormalities, fine motor in-coordination, speech and swallowing difficulties, visual abnormalities, increased fatigue, and cognitive and mood problems. Ataxia types include episodic ataxia, idiopathic ataxia, ataxia telangiectasia, oculo-motor apraxia, vitamin E deficiency ataxia, and COQ10 deficiency ataxia. Freidrich’s ataxia is an autosomal recessive variety. SCA is an autosomal dominant cerebellar ataxia. It has subtypes 1, 2 and 3; SCA 7 is a slightly different type where vision abnormalities precede the ataxia.
There is currently no cure for neurodegenerative disorders; conservative treatment is mainly symptomatic and supportive in nature. Vitamins and supplements are given to help reduce symptoms or slow down the rate of progression of the disease. Occupational therapy and physiotherapy are given to maintain muscle strength and tone. Medications are given to reduce anxiety, induce sleep, reduce pain and twitching, increase blood supply to the brain, and to help balance neurotransmitters.
In this scenario, Ayurvedic treatment has a special role to play in the comprehensive management and control of neurodegenerative diseases. Preclinical and clinical studies have conclusively shown that herbal medicines bring about autoimmune modulation and neuro-protection; reduce inflammation in nerve cells; reduce mitochondrial damage; and possess antioxidant properties.
Ayurvedic treatment is therefore very useful in improving general body immunity as well as specific immunity of the nervous system. Ayurvedic medicines strengthen the nervous system and bring about immunomodulation where there are definite signs of immune mediated damage. Herbal medicines reduce abnormal protein synthesis and aggregation, and help remove abnormal protein deposits. These medicines also help reduce nerve inflammation and help repair and reduce demyelination. Ayurvedic treatment helps improve muscle strength, tone, and neuromuscular coordination; helps rebuild damaged nerves and damaged and dysfunctional parts of the brain; modulates and halts programmed cell death of nerve cells; reduces and reverses mitochondrial dysfunction and genetic mutation; and also helps reduce damage due to the hereditary component of nerve degeneration.
Currently, scientific treatment of neurodegenerative disorders with Ayurvedic medicines is still in the infancy stage, with drug regimes being planned more on a clinical basis to treat functional impairment. This approach is reaping good dividends; affected individuals – with a previous lack of response to all medications – have started improving at a significant pace. Hopefully – in the near future – specifically targeted treatments will emerge, which will treat and reverse damage in specific parts of the nervous system. This will help expedite treatment results, and identify uniform treatment approaches, which in turn will help reduce the devastating effects these diseases have on affected individuals, and hopefully bring about a complete remission.