Bitter melon has antiviral, antimalerial, cardioprotective, and neuroprotective properties. Bitter melon is potentially an important dietary tool for combating insulin resistance, diabetes and obesity. This blog entry reviews the relevant research.
Bitter melon (BM) is one of those strange-looking fruits or vegetables that cause wonderment in me when I see them in Chinese, Indian or third-world markets. It looks like a thin green squash with an extremely bumpy surface. “Momordica charantia, called bitter melon or bitter gourd in English, is a tropical and subtropical vine of the family Cucurbitaceae, widely grown in Asia, Africa, and the Caribbean for its edible fruit, which is among the most bitter of all fruits. There are many varieties that differ substantially in the shape and bitterness of the fruit(ref).” Bitter melon is known by many names including “melao de sao caetano, bittergourd, balsam apple, balsam pear, karela, k’u kua kurela, kor-kuey, ku gua, pava-aki, salsamino, sorci, sorossi, sorossie, sorossies, pare, peria laut, and peria(ref)”
Bitter melon has very complex constituent substances. “The plant contains several biologically active compounds, chiefly momordicin I and II, and cucurbitacin B. The plants contains also several bioactive glycosides (including momordin, charantin, charantosides, goyaglycosides, momordicosides) and other terpenoid compounds (including momordicin-28, momordicinin, momordicilin, momordenol, and momordol). It also contains cytotoxic (ribosome-inactivating) proteins such as momorcharin and momordin.(ref)”
Momordica charantia (bitter melon, BM) is widely cultivated in Asia, Africa and South America for both food and medicinal purposes and is a staple of traditional Okinawan diet. It is “extensively used in Ayurvedic and Chinese medicines as a remedy for diabetes and its complications including neuropathy (ref).” While Bitter melon has long been used as a folk remedy, it has in recent years come under the scrutiny of scientific studies related contemporary Western medicine, and that is the focus of this blog entry.
Animal studies show bitter melon can combat insulin resistance induced by high-fructose diets.
A major current cause of insulin resistance, hyperglycemia and obesity in children is associated by frequent consumption of soft drinks and multiple foods containing large amounts of high-fructose corn syrup(ref)(ref). The 2009 publication Momordica charantia extract on insulin resistance and the skeletal muscle GLUT4 protein in fructose-fed rat reports “We investigated the preventive effect of Momordica charantia Linn. (Cucurbitaceae) fruit, commonly known as bitter melon, on hyperglycemia and insulin resistance in rats fed with a fructose-enriched diet. — First, rats were divided randomly into two groups: the control group was fed with control diet, whereas the experimental group was fed with a 60% high-fructose diet for 8 weeks. After the first 6 weeks, the fructose-treated rats were further subdivided into six groups and were orally fed with or without Momordica charantia L. or rosiglitazone (ROS) for 2 weeks while rats were still on fructose diet. RESULTS: We demonstrated that bitter melon was effective in ameliorating the fructose diet-induced hyperglycemia, hyperleptinemia, hyperinsulinemia, and hypertriglyceridemia as well as in decreasing the levels of free fatty acid (FFA) (P<0.001, P<0.05, P<0.05, P<0.05, P<0.05, respectively). Bitter melon reversed fructose diet-induced hypoadiponectinemia (P<0.05), which provides a therapeutic advantage to insulin resistance in improving insulin sensitivity. Additionally, bitter melon decreased the weights of epididymal (P<0.05) and retroperitoneal white adipose tissue (WAT) (P<0.05). Bitter melon increased the expression of peroxisome proliferator-activated receptor gamma (PPAR gamma) in white adipose tissue (WAT). Conversely, bitter melon decreased the expression of leptin in WAT. Furthermore, we demonstrate that bitter melon significantly increases the mRNA expression and protein of glucose transporter 4 (GLUT4) in skeletal muscle. CONCLUSIONS: This study demonstrates, for the first time, the beneficial effects of two different extracts of bitter melon on insulin resistance in rats fed a high-fructose diet thereby producing evidence of the role of changes in expression of PPAR gamma and GLUT4.”
Also, animal studies show bitter melon can combat insulin resistance and obesity due to consuming a high-fat diet.
The 2003 publication Bitter melon (Momordica charantia) reduces adiposity, lowers serum insulin and normalizes glucose tolerance in rats fed a high fat diet reports: “Bitter melon (BM) is known for its hypoglycemic effect but its effect on rats fed a hyperinsulinemic high fat diet has not been examined. In a dose-response (0.375, 0.75 and 1.5%) study, oral glucose tolerance was improved in rats fed a high fat (HF; 30%) diet supplemented with freeze-dried BM juice at a dose of 0.75% or higher (P < 0.05). At the highest dose, BM-supplemented rats had lower energy efficiency (P < 0.05) and tended (P = 0.10) to have less visceral fat mass. In a subsequent experiment, rats habitually fed a HF diet either continued to consume the diet or were switched to a HF+BM, low fat (LF; 7%) or LF+BM diet for 7 wk. BM was added at 0.75%. Final body weight and visceral fat mass of the two last-mentioned groups were similar to those of rats fed a LF diet for the entire duration. Rats switched to the HF+BM diet gained less weight and had less visceral fat than those fed the HF diet (P < 0.05). The addition of BM did not change apparent fat absorption. BM supplementation to the HF diet improved insulin resistance, lowered serum insulin and leptin but raised serum free fatty acid concentration (P < 0.05). This study reveals for the first time that BM reduces adiposity in rats fed a HF diet. BM appears to have multiple influences on glucose and lipid metabolism that strongly counteract the untoward effects of a high fat diet.”
The 2008 publication Effects of Momordica charantia on insulin resistance and visceral obesity in mice on high-fat diet reports “We examined the preventive effect of Momordica charantia L. fruit (bitter melon) on hyperglycemia and insulin resistance in C57BL/6J mice fed with a high-fat (HF) diet. Firstly, mice were divided randomly into two groups: the control group was fed low-fat (LF) diet, whereas the experimental group was fed with a 45% HF diet last for 12 weeks. After 8 week of induction, the HF group was subdivided into six groups and was given orally with or without M. charantia or rosiglitazone 4 weeks afterward. We demonstrated that bitter melon was effective in ameliorating the HF diet-induced hyperglycemia, hyperleptinemia, and decreased the levels of blood glycated hemoglobin (HbA1c) and free fatty acid (FFA) (P<0.01, P<0.05, P<0.05, respectively), whereas increased the adipose PPARgamma and liver PPARalpha mRNA levels. Additionally, bitter melon significantly decreased the weights of epididymal white adipose tissue and visceral fat, and decreased the adipose leptin and resistin mRNA levels. — It is tempting to speculate that at least a portion of bitter melon effects is due to be through PPARgamma-mediated pathways, resulting in lowering glucose levels and improving insulin resistance, and partly be through PPARalpha-mediated pathways to improve plasma lipid profiles. This is the first report demonstrating that bitter melon, is a food factor, but not a medicine, itself could influence dual PPARalpha/PPARgamma expression and the mediated gene expression, is effective in ameliorating insulin resistance and visceral obesity.”
Rosiglitazone (brand name Avandia) is an antidiabetic drug with serious potential side effects(ref). These studies show that bitter melon’s effects do not depend on rosiglitazone. The 2009 publication Serum sialic acid changes in non-insulin-dependant diabetes mellitus (NIDDM) patients following bitter melon (Momordica charantia) and rosiglitazone (Avandia) treatment states “Comparison of serum sialic acid concentration of patients, following bitter melon and rosiglitazone treatment revealed no significant difference but the study showed that bitter melon could be more effective in the management of diabetes and its related complications as compared to rosiglitazone.”
PPAR-alpha and PPAR-gamma gene expression are briefly characterized in the blog entry PGC-1alpha and exercise.
Important recent research is elucidating the gene-activating mechanisms of bitter melon.
For example, a 2011 study relates to the effect of BM on PPAR-gamma and on the expression of NF-kabbaB: Dietary bitter melon seed increases peroxisome proliferator-activated receptor-γ gene expression in adipose tissue, down-regulates the nuclear factor-κB expression, and alleviates the symptoms associated with metabolic syndrome. “The objective of this study was to examine the extent to which bitter melon seed (BMS) alleviates the symptoms associated with metabolic syndrome and elucidate the mechanism by which BMS exerts beneficial effects. Three-month-old female Zucker rats were assigned to following groups: lean control (L-Ctrl), obese control (O-Ctrl), and obese + BMS (O-BMS). The control groups were fed AIN-93M purified rodent diet, and the O-BMS group was fed AIN-93M diet modified to contain 3.0% (wt/wt) ground BMS for 100 days. After 100 days of treatment, BMS supplementation in the obese rats lowered the total serum cholesterol by 38% and low-density lipoprotein-cholesterol levels by about 52% and increased the ratio of serum high-density lipoprotein-cholesterol to total cholesterol compared to the O-Ctrl group. The percentage of total liver lipids was about 32% lower and serum triglyceride levels were 71% higher in the O-BMS group compared to the O-Ctrl group. Serum glucose levels were significantly lowered partly because of the increase in the serum insulin levels in the BMS-based diet groups. BMS supplementation increased the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) in the white adipose tissue of the obese rats significantly (P < .05) and down-regulated the expression of PPAR-γ, nuclear factor-κB (NF-κB), and interferon-γ mRNA in heart tissue of the obese rats. The findings of this study suggest that BMS improves the serum and liver lipid profiles and serum glucose levels by modulating PPAR-γ gene expression. To our knowledge, this study for the first time shows that BMS exerts cardioprotective effects by down-regulating the NF-κB inflammatory pathway. of operation of bitter melon.” The importance for longevity of downregulation of the NF-kappaB inflammatory pathway is discussed at length in my treatise ANTI-AGING FIREWALLS – THE SCIENCE AND TECHNOLOGY OF LONGEVITY.
The 2008 publication Bitter melon (Momordica charantia L.) inhibits adipocyte hypertrophy and down regulates lipogenic gene expression in adipose tissue of diet-induced obese rats reports: “Bitter melon (Momordica charantia; BM) has been shown to ameliorate diet-induced obesity and insulin resistance. To examine the effect of BM supplementation on cell size and lipid metabolism in adipose tissues, three groups of rats were respectively fed a high-fat diet supplemented without (HF group) or with 5 % lyophilised BM powder (HFB group), or with 0.01 % thiazolidinedione (TZD) (HFT group). A group of rats fed a low-fat diet was also included as a normal control. Hyperinsulinaemia and glucose intolerance were observed in the HF group but not in HFT and HFB groups. Although the number of large adipocytes (>180 microm) of both the HFB and HFT groups was significantly lower than that of the HF group, the adipose tissue mass, TAG content and glycerol-3-phosphate dehydrogenase activity of the HFB group were significantly lower than those of the HFT group, implying that BM might reduce lipogenesis in adipose tissue. Experiment 2 was then conducted to examine the expression of lipogenic genes in adipose tissues of rats fed low-fat, HF or HFB diets. The HFB group showed significantly lower mRNA levels of fatty acid synthase, acetyl-CoA carboxylase-1, lipoprotein lipase and adipocyte fatty acid-binding protein than the HF group (P < 0.05). These results indicate BM can reduce insulin resistance as effective as the anti-diabetic drug TZD. Furthermore, BM can suppress the visceral fat accumulation and inhibit adipocyte hypertrophy, which may be associated with markedly down regulated expressions of lipogenic genes in the adipose.”
Note that some of the beneficial effects of bitter melon taken in conjunction with high fat or high-sucrose diets can be realized through ingestion of other dietary substances such as fish oil(ref)(ref)(ref). The 2009 report A systematic review of the efficacy and safety of herbal medicines used in the treatment of obesity concludes “–compounds containing ephedra, CQ, ginseng, bitter melon, and zingiber were found to be effective in the management of obesity. Attention to these natural compounds would open a new approach for novel therapeutic and more effective agents.”
A number of additional publications report on bitter melon, insulin resistance and weight management including Momordica charantia (bitter melon) reduces plasma apolipoprotein B-100 and increases hepatic insulin receptor substrate and phosphoinositide-3 kinase interactions (2008), Extracts of Momordica charantia suppress postprandial hyperglycemia in rats (2007), Reduced adiposity in bitter melon (Momordica charantia) fed rats is associated with lower tissue triglyceride and higher plasma catecholamines (2005), Reduced adiposity in bitter melon (Momordica charantia)-fed rats is associated with increased lipid oxidative enzyme activities and uncoupling protein expression (2005) and The effects of bitter melon (Momordica charantia) on serum and liver triglyceride levels in rats (2004).
Bitter melon appears to be an antagonist to cancers.
The 2010 publication Bitter melon: antagonist to cancer reports: “The incidence of cancer is increasing worldwide, in spite of substantial progress in the development of anti-cancer therapies. One approach to control cancer could be its prevention by diet, which inhibits one or more neoplastic events and reduces cancer risk. Dietary compounds offer great potential in the fight against cancer by inhibiting the carcinogenesis process through the regulation of cell homeostasis and cell-death machineries. For centuries, Ayurveda (Indian traditional medicine) has recommended the use of bitter melon (Momordica charantia) as a functional food to prevent and treat diabetes and associated complications. It is noteworthy to mention that bitter melon extract has no-to-low side effects in animals as well as in humans. The anti-tumor activity of bitter melon has recently begun to emerge. This review focuses on recent advancements in cancer chemopreventive and anti-cancer efficacy of bitter melon and its active constituents. Several groups of investigators have reported that treatment of bitter-melon-related products in a number of cancer cell lines induces cell cycle arrest and apoptosis without affecting normal cell growth. Therefore, the effect of bitter melon should be beneficial for health, and use of the non-modified dietary product is cost effective.”
The 2010 publication Bitter melon (Momordica charantia) extract inhibits breast cancer cell proliferation by modulating cell cycle regulatory genes and promotes apoptosis reports “Breast cancer is one of the most common cancers among women in the United States. Although there are effective drugs for treating advanced stages of breast cancers, women eventually develop resistance. One of the approaches to control breast cancer is prevention through diet, which inhibits one or more neoplastic events and reduces cancer risk. In this study, we have used human breast cancer cells, MCF-7 and MDA-MB-231, and primary human mammary epithelial cells as an in vitro model to assess the efficacy of bitter melon (Momordica charantia) extract (BME) as an anticancer agent. BME treatment of breast cancer cells resulted in a significant decrease in cell proliferation and induced apoptotic cell death. Apoptosis of breast cancer cells was accompanied by increased poly(ADP-ribose) polymerase cleavage and caspase activation. Subsequent studies showed that BME treatment of breast cancer cells inhibited survivin and claspin expression. Fluorescence-activated cell sorting analysis suggested that MCF-7 cells treated with BME accumulated during the G2-M phase of the cell cycle. Further studies revealed that BME treatment enhanced p53, p21, and pChk1/2 and inhibited cyclin B1 and cyclin D1 expression, suggesting an additional mechanism involving cell cycle regulation. Together, these results show that BME modulates signal transduction pathways for inhibition of breast cancer cell growth and can be used as a dietary supplement for prevention of breast cancer.”
Bitter melon can inhibit colon-cancer causing mutations
The 2001 publication Inhibitory effects of bitter melon (Momordica charantia Linn.) on bacterial mutagenesis and aberrant crypt focus formation in the rat colonreports “Antimutagenicity and chemopreventive activity of an 80%-ethanol extract of bitter melon (Momordica charantia Linn.) against the formation of azoxymethane (AOM)-induced aberrant crypt foci (ACF) was investigated. The bitter melon extract was nonmutagenic and inhibited the mutagenicity of heterocyclic amines 2-amino-3,4-dimethylimidazo[4,5-f]quinoline and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, and aflatoxin B1 in the Salmonella mutation assay. To examine the inhibitory effect of bitter melon on AOM-induced ACF formation, male F344 rats were fed various concentrations of the extract (0.1, 0.5, and 1.0 g/kg body weight) for five weeks during the initiation stage. One week after the administration of the plant extract, rats were subcutaneously given AOM at 15 mg/kg body weight once a week for two weeks. — Treatment with bitter melon extract significantly inhibited ACF formation in the colon during the initiation stage and dose-dependently decreased the average of O6-meG DNA adduct in the colonic mucosa. During the postinitiation stage, bitter melon extract, at 1.0 g/kg body weight, significantly inhibited ACF formation in the colon, especially the formation of ACF with four or more crypts per focus. These findings suggest that bitter melon is a possible chemopreventive agent against colon carcinogenesis.”
Bitter melon appears to have antiviral properties.
For one thing, BM appears to inhibit the HIV virus. See HIV Inhibitor from Thai Bitter Gourd (2001). Also, there is a long history of bitter melon being used as an antiviral in folk medicine. See for example Ethnomedicinal uses of Momordica charantia (Cucurbitaceae) in Togo and relation to its phytochemistry and biological activity.
Bitter melon can protect against certain forms of stress.
The 2009 publication Bitter melon protects against lipid peroxidation caused by immobilization stress in albino rats reports “In the present study, protective effects of bitter melon (Momordica charantia) extract on lipid peroxidation induced by immobilization stress in rats have been assessed. Graded doses of extract (50, 100, and 150 mg/kg body weight) were administered orally to rats subjected to immobilization stress for two hours for seven consecutive days. Stress was applied by keeping the rats in a cage where no movement was possible. — Results reveal that in vivo M. charantia inhibited stress-induced lipid peroxidation by increasing the levels of reduced glutathione and activities of catalase. These results were further supported by in vitro results. In vitro inhibition of lipid peroxidation was indicated by low levels of thiobarbituric acid in the liver homogenate from pretreated rats and normal rats when incubated with both cumene hydroperoxide and extract. Inhibition was also noted in the homogenate where the rats were pretreated but the mixture contained no extract. Thus this plant provides protection by strengthening the antioxidants like reduced glutathione and catalase. Inclusion of this plant in the daily diet would be beneficial.”
Bitter melon is protective against neuroinflammation induced by high-fat diets and works through a variety of pathways.
The June 2011 publication Momordica charantia (bitter melon) attenuates high-fat diet-associated oxidative stress and neuroinflammation looks at obesity-related brain inflammation. “Neuroinflammation is a critical component in the progression of several neurological and neurodegenerative diseases. Increased metabolic flux to the brain during overnutrition and obesity can orchestrate stress response, blood-brain barrier (BBB) disruption, recruitment of inflammatory immune cells from peripheral blood and microglial cells activation leading to neuroinflammation. The lack of an effective treatment for obesity-associated brain dysfunction may have far-reaching public health ramifications, urgently necessitating the identification of appropriate preventive and therapeutic strategies. The objective of our study was to investigate the neuroprotective effects of Momordica charantia (bitter melon) on high-fat diet (HFD)-associated BBB disruption, stress and neuroinflammatory cytokines. — METHODS: C57BL/6 female mice were fed HFD with and without bitter melon (BM) for 16 weeks. BBB disruption was analyzed using Evans blue dye. Phosphate-buffered saline (PBS) perfused brains were analyzed for neuroinflammatory markers such as interleukin-22 (IL-22), IL-17R, IL-16, NF-κB1, and glial cells activation markers such as Iba1, CD11b, GFAP and S100β. Additionally, antioxidant enzymes, ER-stress proteins, and stress-resistant transcription factors, sirtuin 1 (Sirt1) and forkhead box class O transcription factor (FoxO) were analyzed using microarray, quantitative real-time RT-PCR, western immunoblotting and enzymatic assays. Systemic inflammation was analyzed using cytokine antibody array. — RESULTS: BM ameliorated HFD-associated changes in BBB permeability as evident by reduced leakage of Evans blue dye. HFD-induced glial cells activation and expression of neuroinflammatory markers such as NF-κB1, IL-16, IL-22 as well as IL-17R were normalized in the brains of mice supplemented with BM. Similarly, HFD-induced brain oxidative stress was significantly reduced by BM supplementation with a concomitant reduction in FoxO, normalization of Sirt1 protein expression and up-regulation of Sirt3 mRNA expression. Furthermore, plasma antioxidant enzymes and pro-inflammatory cytokines were also normalized in mice fed HFD with BM as compared to HFD-fed mice. – CONCLUSIONS: Functional foods such as BM offer a unique therapeutic strategy to improve obesity-associated peripheral inflammation and neuroinflammation.”
Lack of clinical trial data and cautions
The studies outlined above showing positive health benefits of bitter melon are mainly based on biological activities and small-animal studies and are not large-scale human clinical trial studies. A few publications call for caution in the medicinal use of bitter melon despite the widespread existing folk use. This situation, typical for readily-available natural substances competing with proprietary drugs, has been pointed out in various publications including ones possibly subsidized by pharma companies. Publications suggesting caution with use of bitter melon or pointing out a need for large-scale human clinical trials of bitter melon and other herbal substances include Bitter melon (Momordica charantia): a review of efficacy and safety (2003), Teratogenic effect of the water extract of bitter gourd (Momordica charantia) on the Sprague Dawley rats (2009), Traditional chinese medicines in treatment of patients with type 2 diabetes mellitus (2011) and Anti-diabetic and hypoglycaemic effects of Momordica charantia (bitter melon): a mini review (2009).
Bitter melon recipes
When telling friends or colleagues about writing this blog entry, the inevitable question I am asked is “How do you cook or eat the stuff?”Fortunately, there appears to be no end to delicious-sounding recipes for bitter melon available online such as: vietnamese bitter melon recipes, bitter melon soup recipes, chinese bitter melon recipes, stuffed bitter melon recipes, bitter melon tea, bitter melon soup, karela recipes, and many others that can be found by digging around.
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And the first high blood pressure drug as it relates to Alzhiemers ==>
Lowers blood pressure, lowers pulse AND age-related memory loss reversed in MONKEYS! GUANFACINE aka tenex
Not it seems rather than using the drug the pharmacy approach is to make a NEW and lightly different drug that may or may not be more effective BUT can get a new patent! Why not? Eric [Almost forgot to post this ]
Age-Related Memory Loss Reversed in Monkeys
It happens to the best of us: you walk into the kitchen to get a cup of coffee but get distracted by the mail, and then forget what you were doing in the first place. Aging makes people particularly vulnerable to this kind of forgetfulness, where we fail to maintain a thought in the face of distractions.
New research from Yale University uncovers cellular changes that seem to underlie this type of memory loss in monkeys, and shows that it can be reversed with drugs. By delivering a certain chemical to the brain, researchers could make neurons in old monkeys behave like those in young monkeys. Clinical trials of a generic drug that mimics this effect are already underway.
The findings support the idea that some of the brain changes that occur with aging are very specific—rather than being caused by a general decay throughout the brain—and can potentially be prevented. “It helps us understand that the age-related changes in the brain are malleable,” says Molly Wagster, chief of the Behavioral and Systems Neuroscience Branch at the National Institute on Aging, which funded the research. “That’s a crucial piece of information, and extremely hopeful.”
In the study, Amy Arnsten and collaborators recorded electrical activity from neurons in a part of the brain called the prefrontal cortex, a region especially vulnerable to aging in both humans and primates. It is vital for our most high-level cognitive functions, such as working memory and the ability to multitask and inhibit distractions. “The prefrontal cortex is a mental sketch pad, keeping things in mind even if nothing in the environment is telling us what to do,” says Arnsten. “It’s the building block of abstract thought.”
Previous research has shown that neural circuits in this region are organized to create a sustained level of activity that is crucial for working memory. “By exciting each other, the neurons are able to maintain information that isn’t currently in the environment,” says Arnsten.
By analyzing activity recorded from young, middle-aged, and old monkeys, the researchers found that the firing rate of the neurons in this area declines with age. They found that other neurons, such as those that respond to cues in the environment, still fired normally even as the monkeys aged. The research was published today in the journal Nature.
Arnsten believes the problem is a stress response gone wrong. During stress, even in young animals, these brain cells are flooded with a signaling molecule called cAMP, which dampens activity by opening potassium channels. (She theorizes that this is an evolutionary adaption that allows the brain to quickly flip control from the prefrontal cortex, “a slow and thoughtful region,” to a more primitive region in time of stress.) Normally, enzymes shut off the stress response and the brain goes back to normal. “But we think that in normal aging, the stress signaling pathway becomes disregulated,” says Arnsten.
The researchers were able to rein in the problem by treating the cells with a drug that blocks the potassium channels. After treatment, brain cells in old monkeys fired more rapidly—just like those in their younger counterparts.
The researchers already knew that giving monkeys this drug systemically, rather than delivering it directly into the brain, could reverse age-related deficits in working memory. A clinical trial of the compound, a generic drug called guanfacine, originally used to treat hypertension, is underway at Yale.
The findings bode well for the prospect of slowing age-related cognitive decline in humans. “The more we learn about the synaptic basis of aging, the more we learn it affects very specific elements of what these neurons can do,” says John Morrison, a neurologist at Mount Sinai School of Medicine. Morrison was not involved in the research. “Once we understand it, we can identify targets and deal with it,” he says.
Now that researchers understand how guanfacine works, they may be able to design drugs that are more powerful or have fewer side effects. Guanfacine can act as a sedative, so people need to slowly build up their tolerance to the drug to avoid this effect.
It’s not yet clear if the work has implications for the more serious memory and brain changes that occur in Alzheimer’s disease and other types of dementia. (Monkeys don’t get Alzheimer’s, so researchers know the memory changes they see in these animals are part of the typical aging process.)
However, Morrison believes that these subtle cellular changes may make the brain more vulnerable to the cell death that occurs in Alzheimer’s. And as researchers begin to explore ways to intervene earlier with Alzheimer’s patients, it may be useful to target these changes early on.
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