Get mental stimulation: Brainy activities stimulate new connections between nerve cells and may even help the brain generate new cells. Read, draw, take classes, and explore new hobbies.
Get physical exercise: Exercise increases the number of blood vessels that bring blood to the region of the brain responsible for thought. It also spurs the development of new nerve cells. In one study, for every mile a woman walked each day, her risk of cognitive decline dropped by 13%.
Improve your diet: A reduced-calorie diet has been linked to a lower risk of mental decline. Also remember your Bs: folic acid and vitamins B6 and B12. These can help lower homocysteine levels. High homocysteine has been linked to an increase risk of dementia.
Improve your blood pressure: High blood pressure in midlife increases the risk of cognitive decline.
Improve your cholesterol: High levels of LDL (“bad” cholesterol) increase the risk of dementia, as do low levels of HDL (“good” cholesterol).
Avoid tobacco: According to one study, smoking doubles the risk of dementia.
Limit alcohol intake: Excessive drinking is a major risk factor for dementia. If you choose to drink, limit yourself to two drinks per day.
Protect your head: Moderate to severe head injuries early in life increase the risk of cognitive impairment.
Build social networks: One study linked frequent social interactions with a 42% reduction in dementia risk.
Alzheimer’s disease (pronounced AHLZ-hi-merz) is a disorder that destroys cells in the brain. The disease is the leading cause of dementia, a condition that involves gradual memory loss, decline in the ability to perform routine tasks, disorientation, difficulty in learning, loss of language skills, impairment of judgment, and personality changes. As the disease progresses, people with Alzheimer’s become unable to care for themselves. The loss of brain cells eventually leads to the failure of other systems in the body. The rate of progression of Alzheimer’s varies from person to person. The time from the onset of symptoms until death ranges from 3 to 20 years. The average duration is about 8 years.
Studies have shown that the greatest known risk for developing Alzheimer’s is increasing age. As many as 10 percent of people 65 years of age and older have Alzheimer’s, and nearly 50 percent of people 85 and older have the disease. A family history of the disease is another known risk. Having a parent or sibling with the disease increases an individual’s chances of developing Alzheimer’s.
The U.S. Food and Drug Administration (FDA) has approved two classes of drugs to treat memory symptoms of Alzheimer’s disease. The first specific Alzheimer medications to be approved were cholinesterase (KOH luh NES ter ace) inhibitors. Three of these drugs are commonly prescribed—donepezil (Aricept®), approved in 1996; rivastigmine (Exelon®), approved in 2000; and galantamine (Reminyl®), approved in 2001. Tacrine (Cognex®), the first cholinesterase inhibitor, was approved in 1993 but is rarely used today because of associated side effects, including possible liver damage.
All of these drugs work by temporarily increasing the brain’s supply of acetylcholine (pronounced ah SEE til KOH lean), a cell-to-cell communication chemical involved in learning and memory that becomes deficient in the Alzheimer brain.
In October 2003, the FDA approved memantine (Namenda®), the first Alzheimer drug that works by regulating the activity of glutamate, another cell-to-cell communication chemical. Some glutamate is needed for learning and memory, but too much can over stimulate and damage nerve cells. Memantine protects brain cells against the effects of excess glutamate.
Alzheimer’s disease (AD) is characterized by the deposition of b-amyloid within the brain and activation inflammatory state of microglial cells associated with the amyloid plaque. Nonsteroidal anti-inflammatory drugs (NSAIDs) are efficacious in reducing the incidence and risk of AD and significantly delaying disease progression. In a research published in Folia Medicine 2004, Researcher showed epidemiological evidence that long-term treatment of patients suffering from rheumatoid arthritis with ibuprofen results in reduced risk and delayed onset of Alzheimer's disease (AD). Ibuprofen, a commonly used over-the-counter nonsteroidal anti-inflammatory drug (NSAID), is a cyclooxygenase (COX)-1 and COX-2 inhibitor as well as a peroxisome proliferator-activated receptor (PPARg) agonist, decreases the production of nitric oxide (NO), protects neurons against glutamate toxicity and decreases the production of proinflammatory cytokines. Ibuprofen crosses the blood brain barrier and suppresses neuritic plaque pathology and inflammation in AD brain. Furthermore, ibuprofen is a potent free radical scavenger, and it could reduce lipid peroxidation and free radical generation.
Recent research done by Alzheimer Research Lab at the Case Western Reserve University School of Medicine has also found NSAIDs to activate the peroxisome proliferator activated receptor gamma (PPAR g ), which regulates inflammatory response. NSAIDs, thiazolidinedione (Diabetes drug), and prostaglandin all act as PPARg agonist which inhibit the b-amyloid stimulated secretion of proinflammatory states by microglia and monocytes. PPARg agonists were also shown to inhibit the b-amyloid-stimulated cytokines such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFa). Furthermore, PPARg agonists is also a cyclooxygenase-2 (COX-2) inhibitor. These new research provide direct evidence that PPARg plays a critical role in regulating the inflammatory responses of microglia and monocytes to b-amyloid. NSAIDs are effective in the treatment of AD because of their inhibitory actions on PPARg, not because they are COX-2 inhibitor. In addition, these PPARg are also effective in inhibiting a broad range of inflammatory responses.
Physicians often prescribe vitamin E because it may block molecular activity contributing to brain cell damage. Other medications may be prescribed to treat such symptoms as agitation, anxiety, depression, and poor sleep.
In a human clinical research done by the Alzheimer institute in Chile, patients with early stage of Alzheimer's Disease (AD) were given 250mg of Paractin or Placebo. Two weeks before the clinical trial, the patients undergo appropriate psychoneurological tests such as the Mini Mental Status Exam (MMSE), the Alzheimer Disease Assessment Scale (ADAS), the Boston Naming Test (BNT), and the Token Test (TT). Neuropsychological tests are repeated on Day 0, 6, weeks and 3 months of the clinical trial. Patients using placebo show a significant cognitive deterioration, which is a normal course of the disease. Patients treated with Paractin show improvement or no change in scores. The research suggests that Paractin is a potent PPAR g agonist like NSAIDs, which has been shown to inhibit the b-amyloid-stimulated expression of IL-6 and TNF- a , that might have application for the treatment of AD. For more research on Paractin, CLICK HERE.
Tocotrienol (TCT), an alternate to the more common tocopherol (TCP) variety of vitamin E, is making news for its reported ability to protect against stroke and related brain damage. TCT occurs naturally in palm oil and is a common part of the diet in Southeast Asia, where people tend to suffer fewer neurological disorders than Westerners. Researchers at Ohio State University (OSU) in Columbus recently announced results of a study assessing the efficacy of TCT in minimizing stroke-related brain damage, reported in the October 2005 issue of the American Heart Association's Stroke journal
"We have discovered the molecular checkpoint where TCT works to protect neurons from toxic insults," says Chandan Sen, PhD, professor and deputy director of the Davis Heart and Lung Research Institute at OSU. "Tocotrienol has helped us uncover novel mechanisms of stroke-related neurodegeneration," he adds, referring to research focusing on ischemic stroke, caused when a clot in a vessel stops blood flow to the brain.
The study suggests that "the TCT form of natural vitamin E can be part of a regular diet to keep the brain enriched and more prepared to defend itself, particularly for people at a high risk for stroke," says Sen. The OSU researchers also separately observed that the neuroprotective abilities of TCT were more effective than those of TCP.
Research from Ohio State University (OSU; Columbus, OH) suggests that tocotrienol, the TCT form of vitamin E, might be important in the body's defenses against stroke related neurological damage. TCT may also be promising against ataxia, a disease that affects muscle coordination, speech, reflexes, and sensory function.
OSU researchers performed two studies. In the first, rats given moderate oral doses of TCT for 13 weeks before stroke was induced experienced a significant difference in stroke injury compared with hypertensive rats not fed with TCT.
In the second, orally taken TCT was found to be carried to vital organs by a mechanism independent of the currently known pathways involving tocopherol transfer protein (TTP). Oral TCT was efficiently transported to organs of mice deficient in TTP gene. In humans, TTP gene defects cause ataxia.
"One of the most striking features of these findings is that this neuro protective property is seen in a nutrient known to be safe for human consumption," says Chandan Sen, PHD, professor and vice chair of the department of surgery and deputy director of the Davis Heart and Lung Research Institute at OSU.
"Based on our findings that oral TCT may be transported to vital organs in the absence of TTP, it is important to test whether TCT benefits people suffering from defects in the TTP gene," says Sen. The first study appeared in the October 2005 edition of Stroke, and the second was published in the November 15 issue of Free Radical Biology & Medicine.
Omega-3 fatty acids found in flaxseed and fish is good for maintaining brain health as about 60 percent of the brain consists of lipids (fats) which make up the lining, or cell membrane, of every brain cell. The types of fats present in the brain influence its structure and function. How well your mind works depends, in the long run, on what you eat.
Scientists are toasting both black and green teas as a growing body of research suggests that their components may offer cognitive health benefits. A new study by researchers at Douglas Hospital Research Centre (DHRC) in Quebec, published in a recent issue of the European Journal of Neuroscience, reports that regular consumption of either tea may reduce the risk of age-related degenerative brain disorders such as Alzheimer's disease. "Our findings showed that administration of both black and green tea extracts and catechins strongly blocked death of neurons," says Remi Quiron, scientific director of the DHRC. "This is the first study to show this beneficial effect of both black and green tea."
Also supporting the potential role of green tea in preventing and treating Alzheimer's disease is a study by University of South Florida researchers, published last fall in the Journal of Neuroscience. The scientists used extracts of epigallocatechin-3-gallate (EGCG), an antioxidant polyphenol found in green tea that has also been studied for anticancer effects. Mice that received daily EGCG injections had lower buildups of beta-amyloid, a protein that can lead to nerve damage and memory loss like that of Alzheimer's disease.
Researchers also reported that supplements may be the best way to achieve this result, since other substances present in green tea may hinder the EGCG from providing a beneficial effect.
Finally, a study published in the April 2006 issue of the Journal of Nutrition suggests that green tea catechins may help boost learning ability related to reference and working memory. Japanese researchers studied the effects of green tea extracts on the cognitive learning ability of rats, using a concentration of catechins classified as 63% EGCG, 11 % epicatechin, 6% epigallocatechin, and 6% 'epic ate chin gallate.
Vinpocetine is a derivative of the alkaloid vincamine, found in the periwinkle plant. This unique compound has been dubbed a “cerebral Vasodilator: due to its ability to promote blood flow and metabolism in the brain, thereby enhancing cognitive performance. Moreover, it also has neurological benefits and antioxidant properties and is widely used throughout Europe, Japan, and Mexico (Handler, 2001)
In a study published in the journal Angiology, 20 subjects who were over the age of 60 were given Vinocetine three times a day for two months. At the conclusion of the study, the researchers gauged the subjects’ cerebral blood flow using an ultrasonic Doppler technique and found the blood flow in the carotid artery, which flows to the brain, was favorably impacted, suggesting benefits for brain function. (Miyazaki 1995)
In a double-blind, placebo-controlled study conducted at the University of Graz in Austria, Vincamine was given to 142 participants between 50 and 85 years old twice a day for 12 weeks. At the end of the study period, patients were evaluated using four criteria, including standardized assessment tests and their level of “need for help” from nurses. The results of these analyses indicated that vincaine significantly outperformed the placebo in those with mold for moderate cognitive issues. (Fischhof 1996)
Acetyl- L- Carntitine (ALC) is a transport molecule involved in brain metabolism, including the conversion of long-chain fatty acids into ATP (the building blocks of energy). It assists the production of the vital neurotransmitter acetylcholine. In a double-blind study of 30 ex-alcoholics aged 30 to 60, participants were given two grams of ALC a day for three months. Subsequent tests of their memory, visual spatial capacity, and vocabulary recall showed marked benefits compared with baseline results (Kidd 1999)
Researchers believe that the onset of muddled thinking begins with the development of beta-amyloid plaques in the brain due to oxidative stress that increase with age. To investigate the possible therapeutic impact of ALC on brain health, researchers at the University of Kentucky at Lexington exposed cultures of nerve cells to a beta-amyloid peptide, but one set of cultures was pretreated with ALC. Compared to the controls, the pretreated cultures showed far less free radical debris buy way of protein oxidation, lipid peroxidation, and cell toxicity. (Abdul 2006)
L-Tyrosine and Pyroglutamic Acids: Amino acids are vital for the structure an function of cells that comprise proteins. Two that are especially important for brain health are L-tyrosine and pyroglutamic acid. L-tyrosine is found in small amounts in vegetable and animal protein and fermented foods like miso and yogurt. (handler 2001) It is a precursor of the neurotransmitters epinephrine, norepinephrine, and dopamine, hence its significance for healthy cerebral function and mood, And because of its ability to promote adrenaline levels, it can also help the body cope with stress. (Braverman 1987)
Pyroglutamic acid occurs naturally in various fruits, vegetables, dairy products, and meats but it is also abundant in the brain and cerebrospinal fluid. It has been shown to benefit alcohol-related memory problems and age-related memory concerns (Dean 1990). Researchers at the University of Catania, Italy, enrolled 40 subjects aged 60 to 80 up a double-blind, placebo-controlled, randomized study. The subjects underwent a series of test., including word recall, face recognition, and sequence replication, and were then given either pyroglutamic acid (PCA) or a placebo each day for 60 days. When retested at the end of the study period, the test group scored significantly better than it had at baseline, while the controls showed no change. The researchers concluded that PCA benefited cognitive performance, though they were uncertain as to the exact mechanism of action (Gioli 1990)
Choline: The nutrient Choline is a precursor of the key neurotransmitter acetylcholine and a major constituent of the phospholipids that form cell membranes, including those of brain cells. In a study in which healthy males were fed a choline-deficient diet, levels of phosphatidylcholine, an important phospholipid for brain cell membranes, were observed to drop markedly (Zeisel 1991). In another study, researchers in China gathered 22 patients experiencing age –associated cognitive concerns an performed an assessment of their mental state. Cerebrospinal fluid from these people was then analyzed and found to contain drastically lower concentrations of acetylcholine compared with controls (Jia 2004). This suggests that supplements with its precursor, choline, could be beneficial, as it is able to cross the blood-brain barrier.
Gevuina Oil, also, known as Chilean hazel nut that are high in essential fatty acids such as omega 3, 6, 7 and 9. Gevuina oil is the healthiest oil in the world. Gevuina oil contains about 80% of mono-unsaturated fatty acids (40%-55% Omega 9, 20%-27% Omega 7, 6%-15% Omega 6, and 2% Omega 3), Vitamin E (a-tocotrienol), b-carotein, fitoesterols and a number of other amino acids. Gevuina Oil also contains 7-10% of DHA, which is commonly found in marine fish oil which may help maintain healthy membranes cells and brain health. DHA is an important component of brain tissue. DHA is an omega-3 long chain fatty acid that is the primary building block of the brain and retina. The brain is 60% fat, and DHA is the most abundant fatty acid in the brain, comprising 25-35%. DHA also has been associated with optimal memory function, visual acuity, and a positive mental state. It is an integral component of all membranes with electrical activity, including brain and nerve cells.