When you have a neurodegenerative disease, your neurons or nerve cells degenerate and gradually die before their time. Since neurons don’t divide, no new neurons are formed. As a result, you progressively lose all the functions that these neurons controlled.
The most common neurodegenerative diseases are Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease.1 Research has found that ashwagandha, an Indian herb, helps prevent and manage the symptoms of both Alzheimer’s and Parkinson’s. Ashwagandha is also used in various Ayurvedic preparations to treat Huntington’s.
Before learning why you should use ashwagandha for Alzheimer’s and Parkinson’s disease, let’s understand the conditions.
Alzheimer’s disease is the most common type of dementia where the patient, usually above 65, progressively loses memory and has behavior issues.
Alzheimer’s disease (AD) causes memory loss and behavior issues due to the damage of brain cells – it is the most common type of dementia. With the death of the brain cells, the symptoms worsen over time.
In the later stages, patients can lose their ability to respond to the environment – for instance, carrying on a conversation. Alzheimer’s is usually associated with aging. It typically affects people above 65 years of age. But early-onset Alzheimer’s has been known to happen to those in their 40s and 50s too.
Risk factors mainly include genetics and family history, but head trauma and brain and heart disorders have been linked to Alzheimer’s as well.
Parkinson’s disease (PD) is a slow-progressing degenerative disorder of the central nervous system that affects movement, muscle control, and balance. Even today, it remains an incurable condition.
Parkinson’s disease is caused by the death of dopamine-producing cells. As dopamine helps control body movements, PD patients cannot control their movements or balance.
Brain cells in a part of the brain called substantia nigra produce the neurotransmitter dopamine. Dopamine relays messages to other parts of the brain to control body movements. It is also responsible for emotions like pleasure. In PD, these dopaminergic cells die.
With decreasing dopamine, you would have decreasing ability to regulate your movements, balance, and emotions. Current research suggests that non-motor symptoms like loss of sense of smell (hyposmia), sleep disorders, and constipation may precede the motor symptoms by several years.2
Risk factors include genetic and environmental factors, mainly industrial chemicals like specific insecticides, fungicides, pesticides, and neurotoxins like MTBT.
Causes Of Nerve Damage
Neurodegenerative diseases are characterized by the accumulation of protein clumps in the brain. This typically happens because of the misfolding of certain proteins. These clumps of protein damage the neurons and kill them and lead to the loss of synapses between nerve cells. What this means is that fewer messages are passed between nerve cells. As a result, muscle functions and memory are progressively lost.
In both AD and PD, two different types of protein fragments accumulate outside the nerve cells, building plaques and spherical clumps, and damage these cells.
In AD, protein fragments called beta-amyloid 42 accumulate outside the nerve cells and build up amyloid plaque, which eventually leads to death of nerve cells.3
In PD, the protein alpha-synuclein accumulates to form spherical clumps called Lewy bodies, which is linked to the death of dopamine-producing neurons.4
The normal neuron networks in the brain help in carrying information through their internal transport systems called microtubules. However, in AD, a protein called tau accumulates within the neurons and forms threads which twist abnormally and form tangles. This hinders the transport of nutrients and other essential materials and leads to brain cell damage, causing a variety of effects on human behavior.5
Neurodegenerative Mechanisms May Be Interconnected
Worryingly, the mechanisms of formation of alpha-synuclein Lewy bodies, beta-amyloid plaques, and tau tangles seem to be interconnected. It’s likely that each of these promotes the aggregation and accumulation of the other two and accelerates the progression of the diseases.6
A patient with PD is more likely suffer from dementia than the general population. About 50% of patients with parkinson’s disease dementia also have Alzheimer’s.
Many patients of PD also suffer from dementia; such cases are termed PD dementia (PDD). The signs of dementia become evident as the alpha-synuclein clumps spread from the brainstem to other areas responsible for functions like memory, emotion, behavior, thought, and language (that is, the limbic and neocortical systems). In fact, up to 50% of patients with PDD also develop enough amyloid plaques and tau tangles to be diagnosed with Alzheimer’s.7
Chronic inflammation could also be a direct or indirect cause of neurodegeneration. Neurons are especially vulnerable to free radical attack and a weak neuroimmune system or an exposure to too many free radicals can lead to their death. A study in the International Journal of Neuroscience says that free radicals contribute to neuronal loss in cerebral ischemia and hemorrhage and may be involved in the degeneration of neurons in epilepsy, schizophrenia, tardive dyskinesia, normal aging, Parkinson’s Disease, and Alzheimer’s Disease.8
While AD patients suffer from chronic inflammation, PD patients may suffer from inflammation caused by immune reaction in the parts of the brain affected. And though part of the immune reaction, inflammation can kill nerve cells.
In AD, usually, there is a chronic inflammatory reaction in the brain. In PD, the inflammation may be a local immune reaction in the affected regions of the brain, especially the substantia nigra where the dopamine-producing cells are concentrated. With an increase in cell damage, there is an increase in the number of inflammatory proteins (cytokines), other plasma proteins, and microglial cells, all of which are responsible for immune defense. All of these can lead to the death of neurons.
Anti-inflammatory agents may slow down the progress of dopaminergic cell death in PD and inhibit the onset of dementia.9
Ashwagandha For Alzheimer’s And Parkinson’s Disease
1. Reduces Oxidative Stress And Inflammation
The withanolides or biologically active steroids in ashwagandha, chiefly Withaferin A and sitoindosides VII-X, help reduce inflammation and stress, modulate immunity, fight aging, and improve cognition.10 In fact, Withaferin A is as effective as hydrocortisone sodium succinate, a common anti-inflammatory medicine, dose for dose.11 This is why it has been considered to be a wonder herb in Ayurveda to improve vitality and strength. How exactly does ashwagandha help?
Ashwagandha has steroids that can hunt down cell-damaging free radicals as well as increase the activity of the natural antioxidants in the body.
By Increasing The Activity Of Natural Antioxidant Enzymes
Your body has a natural antioxidative system which has 3 main enzymes – superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX). Withaferin A has been found to increase these enzymes’ activity in the parts of a rat brain that are responsible for controlling voluntary movement and behavior.12 This reduces oxidative damage caused by free radicals. Mice treated with ashwagandha extract showed improved physiological indicators of PD.13
2. Clears Protein Clumps In The Brain
The accumulation of beta-amyloid proteins in the brain depends on the passage of the protein across the blood-brain barrier (BBB) – a membrane that separates blood from the cerebrospinal fluid. This passage is again controlled by the amount of another protein – a soluble LDL receptor related protein (sLRP) – in the BBB cell surface. sLRP binds with 70–90% of beta-amyloid in blood plasma and keeps it from entering the brain. LRP in the liver, on the other hand, removes beta-amyloid from plasma.14
Ashwagandha increases the number of a certain type of protein that helps clear out beta-amyloid proteins from the brain. This can even reverse the symptoms of Alzheimer’s.
In AD patients, however, both the level of sLRP and the level of binding are low, leading to the buildup of amyloid plaque. Ashwagandha increases the LRP in the liver, which helps clear beta-amyloid proteins from the brain. This even reverses the behavior-related symptoms of Alzheimer’s.15 16
3. Increases Dopamine Levels
As ashwagandha increases dopamine levels and reverses free radical damage, it helps treat PD.
We have already discussed how the lack of dopamine is a major contributing factor to Parkinson’s disease. As seen in animal studies, ashwagandha extract improves dopamine levels and reverses all parameters associated with oxidative stress – that is, the inability of the body to cope with cell damage caused by free radicals. This clearly demonstrates its overall effectiveness against Parkinson’s disease.17 18
4. Reconstructs Neuronal Networks
Ashwagandha can improve memory in AD patients as an active steroid in it can regenerate the damaged parts of a nerve cell and recreate nerve networks.
Neurodegenerative diseases are typically associated with death of neurons and hence loss of synapses. This is what hinders transmission of messages and affects cognitive functions in patients of Alzheimer’s. Ashwagandha has withanolide A that can reconstruct neuronal networks and synapses by regenerating axons and dendrites. In this way, it can even improve memory deficits.19
Ashwagandha Both Prevents And Cures Nerve Damage
Neurodegenerative diseases such as Parkinson’s and Alzheimer’s are a result of damage and death of cells in the brain, typically caused by oxidative stress and inflammation. Ashwagandha, with its potent antioxidant, anti-inflammatory, and nerve-protecting properties, not only helps prevent such damage but also repairs, recovers and heals nerve cells, if damage has already occurred. This makes it a wonderful option to include, either on its own, or as a complementary medicine, in the treatment of often difficult-to-treat diseases of the brain such as Parkinson’s and Alzheimer’s.
|↑1||Protein aggregation and neurodegenerative disease. Nature. 2004.|
|↑2||What is Parkinson’s?. National Parkinson Foundation.|
|↑3||Hardy, John A, Higgins, Gerald A. Alzheimer’s Disease: The Amyloid Cascade Hypothesis. 1992.|
|↑4||Luk, Kelvin C., Victoria Kehm, Jenna Carroll, Bin Zhang, Patrick O’Brien, John Q. Trojanowski, and Virginia M-Y. Lee. “Pathological α-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice.” Science 338, no. 6109 (2012): 949-953.|
|↑5||Tau, tangles, and Alzheimer’s disease. Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease. 2005.|
|↑6||Marsh, Samuel E., and Mathew Blurton-Jones. “Examining the mechanisms that link beta-amyloid and alpha-synuclein pathologies.” Alzheimers Res Ther 4, no. 2 (2012): 11.|
|↑7||Irwin, David J., Virginia M-Y. Lee, and John Q. Trojanowski. “Parkinson’s disease dementia: convergence of [alpha]-synuclein, tau and amyloid-[beta] pathologies.” Nature Reviews Neuroscience 14, no. 9 (2013): 626-636.|
|↑8||Jesberger, James A., and J. Steven Richardson. “Oxygen free radicals and brain dysfunction.” International journal of neuroscience (2009).|
|↑9||McGeer, Edith, Koji Yasojima, and Patrick L. McGeer. “Inflammation and the pathogenesis of Parkinson’s disease.” British Columbia Medical Journal 43, no. 3 (2001): 138-141.|
|↑10, ↑12||Bhattacharya, S. K., Kalkunte S. Satyan, and Shibnath Ghosal. “Antioxidant activity of glycowithanolides from Withania somnifera.” Indian Journal of Experimental Biology 35 (1997): 236-239.|
|↑11||Khare CP. Indian Medicinal Plants–An Illustrated Dictionary. First Indian Reprint, Springer (India) Pvt. Ltd., New Delhi (2007) 717-718.|
|↑13||RajaSankar S, Manivasagam T, Surendran S. Ashwagandha leaf extract: A potential agent in treating oxidative damage and physiological abnormalities seen in a mouse model of Parkinson’s disease. Neuroscience Letters. 2009.|
|↑14||Deane, R., A. Sagare, and B. V. Zlokovic. “The role of the cell surface LRP and soluble LRP in blood-brain barrier Aβ clearance in Alzheimer’s disease.” Current pharmaceutical design 14, no. 16 (2008): 1601-1605.|
|↑15||Sehgal, Neha, Alok Gupta, Rupanagudi Khader Valli, Shanker Datt Joshi, Jessica T. Mills, Edith Hamel, Pankaj Khanna, Subhash Chand Jain, Suman S. Thakur, and Vijayalakshmi Ravindranath. “Withania somnifera reverses Alzheimer’s disease pathology by enhancing low-density lipoprotein receptor-related protein in liver.” Proceedings of the National Academy of Sciences 109, no. 9 (2012): 3510-3515.|
|↑16||[Prakash J, Yadav SK, Chouhan S, Singh SP. Neuroprotective role of Withania somnifera root extract in maneb-paraquat induced mouse model of parkinsonism. Neurochem Res. 2013 May;38(5):972-80. doi: 10.1007/s11064-013-1005-4.]|
|↑17||RajaSankar S, Manivasagam T, Sankar V, Prakash S, Muthusamy R, Krishnamurti A, Surendran S. Withania somnifera root extract improves catecholamines and physiological abnormalities seen in a Parkinson’s disease model mouse. J Ethnopharmacol. 2009 Sep 25;125(3):369-73. doi: 10.1016/j.jep.2009.08.003.|
|↑18||Ahmad M, Saleem S, Ahmad AS, Ansari MA, Yousuf S, Hoda MN, Islam F. Neuroprotective effects of Withania somnifera on 6-hydroxydopamine induced Parkinsonism in rats. Hum Exp Toxicol. 2005 Mar;24(3):137-47.|
|↑19||Kuboyama, Tomoharu, Chihiro Tohda, and Katsuko Komatsu. “Neuritic regeneration and synaptic reconstruction induced by withanolide A.” British journal of pharmacology 144, no. 7 (2005): 961-971.|