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<b>Aged Garlic Extract Protects Against Neurodegenerative Diseases</b>

Aged Garlic Extract Protects Against Neurodegenerative Diseases

by Carmia Borek, PhD

Neurodegenerative diseases are on the rise. The Center for Disease Control and Prevention now lists Alzheimerís disease (AD) as the sixth-leading cause of death in America. After Alzheimerís, Parkinsonís disease is the second most prevalent neurodegenerative disorder and affects roughly one million Americans. Any easy and natural measures we can take to protect our brain health is certainly worth exploring. Surprisingly, aged garlic extract (AGE) is showing promise as a neuro-protective supplement whose protective properties are also closely linked to heart health.The damaging molecules that play a critical role in cardiovascular, cerebrovascular and neurodegenerative diseases are reactive oxygen species (ROS), including free radicals. They are byproducts of normal metabolism and increase during infection and inflammation, high plasma homocysteine and during exposure to exogenous sources, including pollutants, smoking, certain drugs (e.g., acetaminophen) and radiation, including UV radiation from sunlight or other sources.
High LDL cholesterol (the bad cholesterol), especially when modified by peroxidation, promotes a build-up of atherosclerotic plaques that can dislodge and block coronary arteries, causing a heart attack, or, block arteries to the brain, resulting in a stroke. In the latter case a state of ischemia (deprivation of blood supply) triggers neuronal death, with possible consequences of developing dementia, and its most common form, Alzheimerís disease. Hypertension contributes to cognitive decline by increasing the number of fibrillar tangles and Abeta plaques which promote the atrophy of the hypothalamus (a center for memory) as seen in AD. In addition,high blood pressure causes cerebral small-vessel pathology which also promotes brain atrophy. High blood homocysteine is another risk factor for cardiovascular disease, stroke, and dementia,including AD. Studies on people 65 years and older and on young people ages 4 to 18 show that plasma levels of homocysteine increase progressively with age. Excess levels of homocysteine result largely from deficiencies in vitamins B6, B12, and folate. Furthermore, as shown in research conducted by Dr. N. Ide, homocysteine, damages the endothelial cells that line blood vessels and reduces the availability of a blood pressure regulator, nitric oxide (NO).

Garlic is a rich source of antioxidants but may be shunned by many because of the odor that lingers on the breath and skin and its potential to cause digestive disorders when eaten in amounts needed for its health benefits.Many of the health benefits of AGE have been proven to be more effective than those of the fresh bulb. AGE is made by a long process of extraction and aging of organic fresh garlic at room temperature to produce high levels of water-soluble organosulfur compounds including S-allyl cysteine (SAC) and S-allylmercaptocysteineóboth powerful and highly bioavailable antioxidants. Standardized by the stable SAC, AGE has been the choice form of garlic in medical research. Other compounds in AGE with antioxidant activity are some oil-soluble organosulfur compounds, flavonoids, allixin, selenium and saponins.

Antioxidant Effects of AGE The antioxidant and anti-inflammatory effects of AGE lower the risk the doctorsí prescription for healthy living 35 for both neurodegenerative diseases and cardiovascular disease. AGE prevents oxidative damage,lowers LDL cholesterol and elevates the HDL cholesterol (the good cholesterol), inhibits the platelet aggregation and adhesion that play a role in atherosclerosis, prevents the progression of plaque formation in arteries and reduces prostaglandins (hormone-like substances involved in inflammation).AGE lowers homocysteine levels, protecting the endothelia lining of blood vessels from oxidative stress. AGE also increases the production and bioavailability of NO. A single dose of AGE was found to increase NO production by 30 to 40 percent, acting as an anti-athrogenic anti-inflammatory agent as well as increasing vasodilatation, helping to lower blood pressure.

Neuroprotective Effects of AGE AGE and its major component, SAC, have potential to prevent neurodegenerative diseases such as AD and Parkinsonís disease by their antioxidative actions that prevent neuronal death by apoptosis. AGE protects against the neurotoxic and apoptotic effects of free radical-producing beta amyloid peptides that form senile plaques in the brain of AD patients. In addition, AGE and SAC save neurons from apoptosis by blocking the action of the apoptotic enzyme, caspase 3. The effect of AGE in reducing homocysteine is another important protective factor against dementia; studies show that adults with intact cognition, whose homocysteine levels increased over time, had an increased incidence of dementia, including AD. Preclinical research on the effects of AGE in reducing neurodegenerative diseases has used models that are genetically prone to early aging and brain senescence. The experiments sought to find out whether AGE can prevent early steps in mental aging, such as memory loss. In a number of studies, these preclinical models received AGE or its component SAC. The results showed that both AGE and SAC prevented the degeneration of the brainís frontal lobe. Treatment improved learning and memory retention and extended life span. To investigate possible mechanisms that are involved in the observed increased cognition, investigators isolated neurons from the hippocampus area of the brain and grew them in the presence of AGE, SAC, or allixin that is present in AGE. The brain cells showed an unusual ability to grow and branch, which may be linked to the findings that AGE increases learning and cognition.

AGE ImprovesSerotonin Levels Serotonin (5-HT) is a neurotransmitter that is released from a variety of sites in the body, including the central nervous system, where it has an effect on cognitive functions. Learning and memory are strongly influenced by serotonin, as some brain regions strongly involved in cognition, such as the pre-frontal cortex and the hippocampus, are densely innervated by serotonergic neurons.A study from the Pasteur Institute in France reported that AGE might modulate receptors that bind to serotonin and inhibit its release, thus making more serotonin available and helping alleviate some pathological conditions that result from its deficiency, including depression.

AGE and Parkinsonís Disease Parkinsonís disease (PD), the second most common neurodegenerative disorder in the United States, is characterized by a loss of voluntary movement as a result of the death of neurons in an area of the midbrain known as the substantia nigra. The neurons in that area of the brain contain the neurotransmitter dopamine. In Parkinsonís disease, dopamine-transmitting neurons in this area die by apoptosis, triggered by free radicals, that are generated in dopamine metabolism. Recent evidence indicates that the substantia nigra of patients with PD contains increased iron,which enhances oxidation, and decreased glutathione, which protects against the formation of free radicals. Further, the end products of peroxidized lipids are increased in the substantia nigra of patients with PD, supporting the notion that free radicals contribute to dopamine neuronal death. Thus antioxidant therapies may slow the rate of progression of PD. Aged garlic extract, with its high antioxidant capacity, its ability to inhibit lipid peroxidation of membranes, and increase glutathione and antioxidant enzymes in cells, shows promise as a potential preventive and treatment agent in PD. A recent preclinical study found that the SAC component in AGE prevents the effects of the neurotoxic agent MPP (+), that depletes dopamine in the brain and impairs movement, mimicking the pathological state of PD. Pre-treatment with SAC, prior to treating with MPP (+), resulted in decreased oxidant stress. SAC blocked MPP (+)-induced lipid peroxidation, prevented superoxide radical production and increased the activity of the internal antioxidant enzyme superoxide dismutase. Behavioral analyses showed that SAC improved MPP (+)-impaired movement by 35 percent. While clinical studies are needed to confirm the action of SAC in humans, the present study suggests a potential for SAC to help in the prevention and treatment of PD.

Carmia Borek, Ph.D., is the Professor of Public Health and Family Medicine at Tufts University School of Medicine, and a nutrition and health consultant. Her research specialties include the area of antioxidants and health.
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