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Molecules 2014, 19(12), 20864-20879; https://doi.org/10.3390/molecules191220864
Relevance of the Anti-Inflammatory Properties of Curcumin in Neurodegenerative Diseases and Depression
Department of Pharmacology, College of Medicine, Howard University, Washington, DC 20059, USA
Author to whom correspondence should be addressed; Tel.: +1-202-806-9719, Fax: +1-202-806-4453.
Received: 21 October 2014; in revised form: 5 December 2014 / Accepted: 8 December 2014 / Published: 12 December 2014
This review is an attempt to summarize our current understanding of curcumin's potential as a neuroprotectant and an antidepressant. This dual property confers a unique advantage to this herbal medication, believed to be devoid of any major side effects, to combat commonly observed co-morbid conditions of a neurodegenerative and a neuropsychiatric disorder. Moreover, in line with the theme of this series, the role of inflammation and stress in these diseases and possible anti-inflammatory effects of curcumin, as well as its interaction with signal transduction proteins as a common denominator in its varied mechanisms of action, are also discussed. Thus, following a brief introduction of curcumin's pharmacology, we present research suggesting how its anti-inflammatory properties have therapeutic potential in treating a devastating neurological disorder (Parkinson's disease = PD) and a debilitating neuropsychiatric disorder (major depressive disorder = MDD). It is concluded that curcumin, or better yet, an analog with better and longer bioavailability could be of important therapeutic potential in PD and/or major depression.
Keywords:curcumin; inflammation; depression; Parkinson's disease; neuroprotection
1. Curcumin
Curcumin, a diarylheptanoid, is the principal curcuminoid of the popular South Asian spice turmeric (Curcuma longa), which is a member of the ginger family (Zingiberaceae). Curcumin and turmeric's other two curcuminoids, desmethoxycurcumin and bisdesmethoxycurcumin are natural phenols responsible for the yellow color of turmeric. Indeed, because of its bright-yellow color, curcumin is used as a food coloring as well as food additive. Curcumin can exist in several tautomeric forms, however, the enol form is more stable in the solid phase and in solution [1].
Curcumin's antioxidant [2,3,4], hepato- and nephroprotectant [5,6,7], antimicrobial [8,9], anti-inflammatory [10,11,12,13] and potential anti-depressant properties [14,15,16,17,18,19] are well documented. Epidemiological studies have demonstrated that societies that widely use curcumin show reduced incidence of inflammation-influenced and cognitive function diseases such as Alzheimer's disease [20,21,22,23]. It has also been suggested that curcumin may reduce the incidence of Parkinson's disease (PD), as some studies have shown an absence of age-related changes in nigral dopaminergic neurons in Indian populations that consume large amounts of curcumin [24,25,26]. Moreover, as discussed below, numerous in vitro and in vivo studies provide substantial evidence for a protective effect of curcumin against insults that may precipitate PD-like symptoms.
2. Depression
2.1. General Considerations
Major depression is a disorder with many definitions and manifestations and with a 12-month prevalence rate of 6.3% to 10.3% in Western societies [27]. Symptoms may vary, but often include anhedonia, disrupted sleep patterns, lack of motivation, or emotional distress (e.g., anxiety). Although a number of clinically effective treatments are available, a large segment of patients are non-responsive (i.e., exhibit treatment-resistance to first-line interventions: [28,29]). Recent discoveries provide growing support for presence of cellular atrophy and neuronal death in major depressive disorder (MDD) as well as neurotrophic effects associated with antidepressants [30,31,32,33,34]. Thus, converging evidence support neurotrophic effects as a unifying hypothesis for antidepressants efficacy in treating MDD (see [35] for a detailed review). Moreover, activation of the ERK⁄MAPK pathway by antidepressants increases the expression of nuclear CREB, which facilitates the expression of neurotrophic/neuroprotective proteins such as Bcl-2 and brain-derived neurotrophic factor (BDNF). A current hypothesis posits that curcumin alleviates depressive behavior through activation of ERK-Bcl-2-BDNF neurotrophic pathway [36,37,38,39,40], particularly in areas implicated in the pathophysiology of depression (e.g., hippocampus and olfactory system: [41,42,43]).
2.2. Depression-Inflammation
The purpose of inflammation is primarily to remove or inactivate potentially damaging agents or damaged tissues. This response is mediated via one of two cell systems: glia of the central nervous system (CNS), and lymphocytes, monocytes, and macrophages of the hematopoietic system [44,45]. Neuroinflammation is the brain's response to injury, infection, or disease. Although, initial immune or inflammatory response is to remove damaged tissue or to inactivate potentially damaging agents, over-activation of the system can have severe detrimental consequences including precipitation of depressive-like behavior. Thus, patients who have major depressive disorder show alterations in immunologic markers such as increases in pro-inflammatory cytokines (discussed below). Moreover, chronic low-grade inflammation may result in changes in brain structure and synaptic plasticity leading to neurodegeneration [46,47,48,49]. This, coupled with a reduction in neuroprotection, may not only exacerbate depression, but may also lead to dementia, particularly in older people [48,50]. Furthermore, research suggests that neuroinflammation is suppressed by norepinephrine (NE), and that NE uptake inhibitors' therapeutic efficacy in depression may be at least partially related to this mechanism [51]. Interestingly, Interferon-γ (IFN-γ), a cytokine that is critical for innate and adaptive immunity, induces the enzyme indoleamine 2,3-dioxygenase (IDO), which causes reduction in tryptophan availability, leading to a reduction in serotonin synthesis in the brain that has been implicated in depression [52].
3. Cytokines
Cytokines are a large family of small signaling proteins secreted from various cell types that elicit varied biological activities including induction of both anti- or pro-inflammatory responses. Anti-inflammatory cytokines are generally released to counteract the pro-inflammatory cytokines. This regulation helps limit damaging effects of prolonged or excess inflammation caused by the pro-inflammatory cytokines. However, cytokines dysregulation can lead to insufficient mediation or inhibition of normal immune reaction leading to disease manifestation including neurodegenerative diseases (e.g., PD) as well as major depression [53,54,55,56,57,58]. For example, interleukins (IL-1, IL-6), and TNF-α are released in response to various toxins such as lipopolysaccharide (LPS: a compound derived from membrane of gram-negative bacteria causing inflammatory-mediated damage) and typically cause a low-level inflammatory response to combat the insult [59,60]. However, these cytokines tend to have dual effects. For example, IL-6 may not only have a pro-inflammatory action [61,62], but may also act to attenuate or down-regulate synthesis of other pro-inflammatory cytokines (e.g., IFN-γ, IL-1, and TNF-α) [59,63,64]. IL-1, and TNF-α, as mentioned earlier also have acute pro-inflammatory actions, and dysregulation of production of one or more of these cytokines may precipitate a variety of neurological disorders including PD as well as MDD [65,66,67,68]. The mechanism of cytokine actions include impairment of neurogenesis and exacerbation of neuronal death [69,70,71,72,73] and may involve disruption of survival signaling pathways and caspase-dependent cascades, as well as alteration of normal receptor function [71,72,73].
4. Parkinson's Disease
4.1. General Considerations
Parkinson's Disease (PD), the second largest neurological illness in the elderly after Alzheimer's, may affect as many as 6.3 million people worldwide. This neurodegenerative neurological movement disorder mostly affects people over the age of 65, however 15% of people can develop it before the age of 50. PD is a progressive neurodegenerative disorder that causes increased debilitating symptoms resulting from loss or damage to dopaminergic cells in the substantia nigra (SN). The causes for the development and progression of PD invariably involve an interaction between the person's environment and genetic disposition. In fact, many studies link PD with exposure to various endogenous (e.g., salsolinol) and exogenous toxins (e.g., MPTP = 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) (reviewed by [74]). Therefore, these compounds are often used to create in vitro and in vivo models to study PD. Salsolinol is an endogenous neuromodulator in dopaminergic cells formed during the metabolism of dopamine [75]. Dysregulation of salsolinol, especially its (R)-enantiomer form in the brain, is thought to contribute to development of PD [76,77,78,79]. It has been proposed that salsolinol and its derivatives (e.g., norsalsolinol, N-methylnorsalsolinol, N-methylsalsolinol) may serve as a marker for PD as they are increased in the cerebrospinal fluid [80] and the urine [81] of patients with PD. Exogenous compounds that are non-isoquinoline derivatives have also been shown to induce dopaminergic cell death in the SN. One such example is rotenone, a naturally occurring plant toxin that has been developed into a widely used pesticide and insecticide. Rotenone's toxicity has been demonstrated in various in vitro [82,83,84] and in vivo [85] studies. Moreover, it has been shown that when low doses of multiple exogenous factors are combined, a synergistic neurotoxicity may result. Thus, combination of nontoxic or minimally toxic concentrations of rotenone and LPS can result in exaggerated or synergistic toxicity [86]. Recently, we have provided in vitro evidence that exposure to a combination of salsolinol and rotenone can have synergistic toxicity. Moreover, we showed that pretreatment with curcumin can protect against such toxicity [87].
4.2. PD and Inflammation
As mentioned above, the immune system is designed to help protect the body against disease, toxic agents, stress, and injury. Inflammation is the first response to infection and injury as the body initiates a defense, mediated by cytokines towards the healing process. In a normal functioning system, pro- and anti-inflammatory cytokines function in a regulatory loop to maintain the proper response. However, breakdown of the normal response by factors such as stress or other insults can cause inflammation to become persistent and harmful [88]. For example, inflammation induced by LPS causes long-term increase in brain TNF-α from microglia months after it has subsided in the periphery [89]. This increased pro-inflammatory response may also induce a delayed and progressive loss in dopaminergic neurons in the substantia nigra, similar to that seen in PD suggesting that enhanced neuroinflammation could lead to PD [89,90,91]. In addition, the elevated levels of pro-inflammatory cytokines (e.g., IL-6 and IL-1β) can induce symptoms of a syndrome termed "sickness behavior" [89,92,93], which include depression, reduction in locomotor activity, anhedonia, anorexia and cognitive disturbances [92,93,94,95]. In recent years, a number of findings have reinforced the idea that unregulated inflammation can lead to major depression and neurodegeneration. This contention is further supported by the findings that administration of high levels of pro-inflammatory cytokines can cause changes in behavior similar to depression and that attenuation of inflammatory response reduces depressive symptoms [96,97]. Thus, there is substantial support for inflammation as a common neurobiological substrate responsible for the co-morbid manifestation of neurodegenerative diseases (e.g., PD) and MDD. Curiously, it has been recently proposed that inflammation may also be the common mediator of commonly observed co-morbid conditions of depression and chronic pain [93].
5. Role of Stress
Stress is known to alter immune functioning [98]. Maes et al [98] were the first to show that psychological stressors in humans induce inflammatory responses through production of pro-inflammatory cytokines, such as IFN-γ and TNF-α. Subsequent studies have shown this to be true with a variety of other stressors as well [99,100]. Animal studies have also demonstrated that stressors increase cytokine levels such as IL-1beta and IL-6 in the blood and in various regions of the brain [49,69,101,102]. Goshen et al. [69] have specifically shown that after chronic mild stress normal mice show depressive-like behavior and an increase in IL-1β in the hippocampus. However, IL-1 receptor-deficient mice do not show such behavioral changes. Recently, it has been shown that direct administration of TNF-α can also induce a depressive-like state that can be blocked with the anti-TNF-α antibody [103]. Interestingly, it has been proposed that the action of some anti-depressants may also be attributed to a reduction in pro-inflammatory cytokines [97,104]. Moreover, neurological diseases like Alzheimer's disease [50,105], amyotrophic lateral sclerosis, epilepsy, Huntington's disease, multiple sclerosis, and PD [106] are often co-morbid with depression and express inflammatory markers. Thus, stress via enhanced release of pro-inflammatory cytokines such as TNF-α, IL-1β and IL-6 may not only precipitate depression, but may also accelerate the neurodegenerative processes. For this reason drugs that may interfere with detrimental consequences of stress on inflammatory pathways may be of therapeutic potential in neurodegenerative and/or mood disorders.
Thus, direct effects of stress on inflammatory pathways, key proteins involved in signal transduction mechanisms as well as a variety of neurotrophic factors may be a common denominator to the detrimental consequences of chronic stress including induction and/or aggravation of neurodegenerative diseases as well as neuropsychiatric disorders including MDD.
6. Curcumin: Antidepressant
The above discussions have provided a framework for consideration of inflammation as an important player in the precipitation of depressive disorders. Hence, the well-documented anti-inflammatory effects of curcumin in in vitro and in vivo studies [107,108,109,110], including our own observation of its protective effects against LPS- and various cytokine-induced toxicity in SH-SY5Y cells [87] offer a mechanistic basis for observed antidepressant effects of curcumin. Indeed, numerous studies using various animal models of depression [14,15,16,111,112] including olfactory bulbectomized rat model of depression [113] as well as a recent report by us utilizing the WKY rats as a putative animal model of depression [19] provide solid evidence for an antidepressant effect of curcumin. Moreover, various clinical studies indicate therapeutic potential of curcumin in MDDs. These studies include randomized controlled trials of curcumin alone [114,115], or with piperine, an alkaloid found in black and long peppers, to boost the bioavailability of curcumin [116].
7. Curcumin: Neuroprotectant
Similarly, the role of neuro-inflammatory mediators as contributory factors to neurodegenerative diseases in general, and PD in particular, have been emphasized above. Numerous observations of the protective effects of curcumin against various inflammatory-mediated axonal or neuronal damage are all in line with its potential beneficial effects in treating neurodegenerative diseases including PD. For example, research shows its protection against: chronic inflammation associated with Alzheimer's disease [117]; axonal degeneration from local neuroinflammation [118]; β-amyloid induced degeneration [119]; peripheral neuropathy [120]; experimental models of Huntington's disease [121]; okadaic acid induced memory impairment in mice [122]; N-methyl N-nitrosourea induced functional and structural alterations in mice brain [123], as well as our own observation of its protective effects against damage induced by a combination of salsolinol and rotenone in neuroblastoma cell lines [87]. A survey of clinical studies on potential usefulness of curcumin in Alzheimer's disease [124,125]; dementia [126] and PD further support its potential therapeutic benefits [127,128].
8. Conclusions
Based on the above discussion, it is not unreasonable to suggest that the anti-inflammatory properties of curcumin are at least partially responsible for its antidepressant and its neuroprotectant effects. However, a few important points have to be considered in this regard. The first point concerns the bioavailability of curcumin as dietary curcumin exhibits poor bioavailability [129]. This might be due to several factors including its insolubility in water, poor absorption and rapid metabolism that need to be overcome for a more meaningful therapeutic intervention with curcumin. In this regard, it has been suggested that addition of piperine could enhance its absorption [116,129]. Moreover, the bioavailability of curcumin; may be increased by its dissolution in oil or cooking [130]. This is key in understanding the effects seen in the epidemiological studies [24,25,26], as curcumin, piperine, and oil are often used in combination in traditional Indian cooking. However, pharmacological structural modification and development of novel curcumin derivatives that may be administered orally or intra-nasally may offer a more realistic and potent therapeutic approach.
The other important point concerns possible combination of curcumin or its more stable derivatives with current or other medications to treat depression and/or PD. This approach may be particularly beneficial since different drugs may act at different sites and offer a better control of inflammatory and other processes (e.g., oxidation) that may contribute to the pathology of these diseases. In this regard, it is noteworthy that a number of novel compounds including nicotine, resveratrol, ketamine and more recently, estrogen receptor agonists, have shown potential usefulness in major depression and PD [131,132,133].
Finally, it is also of relevance to note that, in addition to the mechanisms mentioned above, curcumin might also affect a variety of other factors or mediators that have a direct role in neurodegenerative and/or mood regulating processes. To this end, it has been demonstrated that curcumin may affect: mitochondrial dysfunction [134]; oxidative stress [135]; molecular chaperones [136]; mTOR pathway [137] and MAPK expression [138]. Figure 1 provides some insight into few possible molecular mechanisms involved in neuroprotective and/or antidepressant effects of curcumin. These mechanisms warrant further research to understand their role in mediating the various actions that curcumin has in the brain.
In summary, novel compounds based on curcumin, alone or in combination with other known drugs that suppress inflammation and have been shown to exert antidepressant and/or neuroprotective effects may offer optimum therapy in major depression and PD.
Figure 1. Potential Molecular Mechanisms Affected by Curcumin. The inhibition of cell signaling pathways such as Akt, NF-κB, or PI3K [139], has been suggested as the mechanism responsible for anticancer effects of curcumin. Curcumin may also inhibit the activity and synthesis of the enzymes implicated in inflammation such as cyclooxygenase-2 and 5-lipooxygenase. Moreover, its anti-inflammatory effect may be linked to inhibition of pro-inflammatory leukotrienes as well as to its neutrophil function [63,64]. Inhibition of TNF [59] may contribute to a physical interaction with other key signaling protein like BDNF that might enhance its antidepressant effect.
This work was supported by a grant from NIH/NIAAA R03AA022479.
Author Contributions
YT in consultation with LH, LA and ZQ designed research. LH, ZQ and LA performed research and with YT analyzed the data. YT, LH, LA and ZQ wrote the paper. All authors read and approved the final manuscript.
Conflicts of Interest
The authors declare no conflict of interest.
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Christie Heywood is a fantastic photographer herself, so it was a privilege when she asked me to photograph the birth of her baby girl.
She called me in the early morning when she went to the hospital but was not dilated very much, so I told her to keep me in the know and keep contacting me throughout. She texted me at 9:58am that she was getting her epidural and felt she was close so I better come. I jumped in my car and headed to the hospital. As I came down the hall, there was a friend outside the door who said "better hurry, they are all in there!" She had gone so quickly after the epidural and things were moving very fast. I hurried in, ran up to the head of the bed and got in place ready to start photographing. I got there right in time. 6 pushes, 2 contractions and out came her gorgeous baby girl! It all happened so fast! She was absolutely perfect and pink.
Not too long after things in the room settled down, Christies two sons came in very excited to see their baby sister. And to give mom a couple snuggles. Their little excited faces were my favorite. They just kept kissing her and staring at her. She's one lucky little girl to have two big brothers to watch over her.
With everything going so quickly, I didn't get a lot of time to get to know Christie and her husband, but I was super glad to be there and be a part of this beautiful day, to see how excited they were for their first little girl and see them snuggle her right up. Congratulations you guys!!
Christie Heywood Birth Story// Logan Regional Hospital // Shanda Call Birth Stories
Christie Heywood is a fantastic photographer herself, so it was a privilege when she asked me to photograph the birth of her baby girl.

subset: commoncrawl


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Tuesday, September 15, 2009
Don't Bring a Crowbar to a Sword Fight
A habitual offender with 29 prior arrests had been released from a year in county jail just days before. He probably had some ideas in mind of what he would do when he got back on the streets. Being confronted by a college student whose garage he was burgling was probably not in his plans. That the student might be armed with a samurai sword probably never crossed his mind. Having his arm chopped nearly off before he died came as a surprise, I expect.
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Wearables have a been consistent staple of this year. Whether it is a smartwatch, a fitness tracker or other health related wearable they are now in abundance. So much so that the choice is almost too much. One of the companies who has released a number of wearable over the last 18 months is FitBit. Generally speaking, their wearables are all health and fitness related although they can tell you the time as well (not sure if that is enough anymore to be called a watch). Anyway, FitBit have become pretty good at releasing these sorts of wearables.
That said, they did have a spot of bother at the start of the year when a number of its users starting having skin irritation issues with the then released FitBit Force. It seems wearing the bands caused quite substantial rashes on some users although FitBit claimed the affected users to be less than 2% of those who bought one. Either way, FitBit were not looking to cause any problems with customers and promptly offered a recall on the units and refunded those who had an issue.
Well, since then FitBit has launched a few more wearables including the recently released FitBit Charge. And you guessed it. This one also seems to be causing some users skin irritation problems. Now in contrast (and as the CEO of FitBit is quick to point out) the number of affected users (so far) is only a handful compared to more than one hundred thousand who have bought the device. That said, FitBit will not want a repeat of what happened with the FitBit Force. As a means of reassurance, the FitBit CEO also advises that a different form of adhesive (which was believed to be the problem with the Force) was used to what was provided in the Force. Further adding the company had met with dermatologists to make sure the current product did not elicit similar issues. In fact, the cause being offered by FitBit is likely a build up of sweat, water and soap being held against the skin underneath the device. As such, regularly cleaning is being touted as a means to avoid the problem. Either way though, if similar cases continue to come to light then this won't be good news for FitBit. Are you a FitBit Charge owner? Noticed any issues with the device? Let us know.


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Written by J.M Wasko On July 11, 1804, Alexander Hamilton found himself in Weehawken, NJ, looking straight down the barrel of a dueling pistol aimed at him by Aaron Burr. This historic moment was frozen in time by artist Kim Crowley in a pair of statues that depicts the moment before shots were fired on…Read More
Independence Day Fun at the New-York Historical Society
July 7, 2016
Written by Shana Fung, The New-York Historical Society's Summer of Hamilton started off with a bang this Fourth of July weekend. On Independence Day, families mingled with Revolutionary War soldiers, ladies from the Founding Era, and Alexander Hamilton himself in between creating tricorne hats, designing festive flags, participating in a singalong with the Hudson River…Read More


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Education on crop protection is key for a more sustainable future
The International Symposium on Crop Protection (ISCP) at Ghent University yearly focuses on the latest innovations in crop protection. For the 69th edition many international universities and some industrial partners, like Eastman, Clariant & Bayer, were present to share their vision on the future of crop protection. All agreed that new technologies and further research on crop protection are crucial to obtain a more sustainable agriculture.
Professor Pieter Spanoghe, the chair of this ISCP, adds education and proper training to that list. He will also organize the IUPAC 2019 global congress on crop protection that will come to Ghent in May 2019. This four-yearly event can be seen as the Olympics in crop protection. The theme will be education, because future researchers, farmers and the general public need to be properly educated globally on the science and use of crop protection.
Crop protection chemistry
An important part of crop protection is the chemistry. Pieter Spanoghe, who is professor in crop protection chemistry at Ghent University (UGent), agreed that chemical crop protection products are extremely useful, and further improving their formulation and application is essential to reduce unwanted side effects on man, animal and the environment. However, the formulation of chemical crop protection products can be tricky sometimes. "It is always a challenge to ensure that crop protection chemicals remain as efficient on the field as they are in the lab", said professor Peter Baur from Clariant Industrial. And that is just one of the many challenges in crop protection that also applies to the new formulation of non-chemical products such as biopesticides.
Crop protection (chemistry) is a very wide subject. There are loads of different approaches to it and a variety of different research is done within the theme. Besides making the products better many researchers study the effects of the products on the environment. One example is the work of associate professor Christopher Cutler from Dalhousie University on the effect called 'hormesis'. That is when a plant grows faster after it has been treated with a small dose of a certain herbicide. Or when a small dose of insecticide has beneficial effects on insects. Apparently the phrase 'What does not kill you, makes you stronger', is not that farfetched after all.
Sharing knowledge
To face the challenges and find better solutions, the academic world and the industry should work together. According to professor Baruch Rubin from the Hebrew University of Jeruzalem, industry and academy should join forces to further develop crop protection. That is also why symposia and congresses like the International Symposium on Crop Protection (ISCP) and IUPAC 2019 are so important. Bringing experts from all over the world together to exchange knowledge can only benefit the agricultural world.
Only by sharing our knowledge with one another, can we further improve technologies in the crop protection world. To tackle the current and upcoming agricultural challenges, we must work together and make sure our knowledge gets passed on to the future generations. They are the ones who will have to conduct more research and find new solutions for future threats. The importance of good training and education can never be underestimated.
Education is key
Ghent University is renowned for its high-quality education and cutting-edge research. Prof. Anne De Paepe, rector of Ghent University hopes that by organising international conferences like the ISCP and IUPAC 2019, Ghent University will maintain and even strengthen its position at the international forefront of science. That is why she also insisted everybody save the date for the IUPAC 2019 congress.
"Innovation in crop protection is a very important subject and it is our duty to educate the current and future generation of researchers and farmers", concluded the rector. Interesting fact-based discussions on crop protection can broaden our minds and interaction with other specialists can give us new insights. But this knowledge also needs to be better translated to the general public in an unbiased way. That is why education is also the theme of the IUPAC 2019 congress.


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Self catering cottage holidays in Moorshop, Devon
There is no better way to explore Moorshop in Devon than a self catering cottage or apartment.
We have a wide range of self catering accommodation available in Moorshop and Devon that are suitable for budgets of all sizes. Whether you are looking for a short break, a romantic escape or a family holiday you will find some excellent self catering in Moorshop.
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Blacksmiths Cottage, Moorshop
Self catering in Devon, South West England
Blacksmiths Cottage is a 'picture postcard' holiday cottage ideally located within the Dartmoor National Park. Lovingly renovated, it has bags of charm and is presented to a very good standard with underfloor heating throughout the ground... more


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The question of who Star-Lord's father actually is dropped as a key story point at the end of Guardians of the Galaxy, but was left to be answered in the now-forthcoming sequel. But if fans thought they were going to have to wait until the film was released to learn the truth, they were mistaken: As part of Marvel's news-filled presentation at San Diego Comic-Con 2016, the new Guardians of the Galaxy Vol. 2 trailer dropped and revealed the unexpected character's identity - and who is portraying him.
As played out in the trailer: Kurt Russell will portray Ego: The Living Planet, and the character has been confirmed as having fathered Peter Quill, aka Star-Lord (Chris Pratt) in writer/director James Gunn's (and the Marvel Cinematic Universe's) version of the Guardians of the Galaxy mythology.
Traditionally portrayed as a (literal) planet whose topographical features form a human face, Ego is a cosmic being from deep space who frequently serves as both a villain, mentor and morally-ambiguous figure in the vast Marvel cosmology. Apart from fathering the franchise's hero (somehow), Ego's form and function in the Marvel Cinematic Universe is unknown - although one of his lines in the trailer (not yet online) is said to have been: "Yes, Drax, I do have a penis."
You can check out the newly-released logo for Guardians of the Galaxy Vol. 2 (which debuted during the Marvel SDCC panel), below.
NEXT: Vulture Confirmed for Spider-Man: Homecoming
Doctor Strange opens November 4, 2016; Guardians of the Galaxy Vol. 2 – May 5, 2017; Spider-Man: Homecoming – July 7, 2017; Thor: Ragnarok – November 3, 2017; Black Panther – February 16, 2018; Avengers: Infinity War Part 1 – May 4, 2018; Ant-Man and the Wasp – July 6, 2018; Captain Marvel– March 8, 2019;Avengers: Infinity War Part 2– May 3, 2019; and as-yet untitled Marvel movies on July 12, 2019, and on May 1, July 10, and November 6 in 2020.
Source: Marvel


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Commissioners meet today
The Churchill County Board of Commissioners meets at 1:15 p.m. today at the Churchill County Administrative Building, Commission Chambers, 155 N. Taylor St., Suite 145.
On the agenda is:
Update of current activities, plans or actions related to the Bureau of Land Management's Carson City District
Update on The Arts Center 5th annual Golf Tournament Fundraiser for the Arts
Approval to enter into an agreement with the State of Nevada, Division of Housing for $30,000 in trust funds to support Rural Nevada Continuum of Care, Social Entrepreneurs, Inc. Homeless Planning Contract.
To possible approve the Churchill County Social Services to enter into PATH Program Leases with Rogne Realty for Dec. 1 to Nov. 30, 2018, totaling $18,000.
To possible approve to allocate 175 acre feet of county-owned water to the Lahontan Valley Bird Dog Club re-vegetation project on Pasture Road
To possible approve a Joinder Contracts with G4S Secure Solutions for Security Services at the Tenth Judicial District Court and the new jail, at a rat $22.57 per hour with an overtime/holiday rate of $31.60 for the remainder of 2017, with an increase to $23.26 per hour and $32.56 per hour in 2018.
Approval of a contract with Hiskett & Sons in the amount of $33,739 to return property on Gummow Drive to prior condition.


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to my partner, it is coming, I promise.
Friday, September 5, 2008
Concering apron swapp
Posted by daurenet at 11:30 PM
3 comments:
- Sibyl said...
Just wondering if you have received my apron as of yet. I mailed it last Thursday.
- September 10, 2008 at 7:41 PM
- Heidi said...
I LOVE LOVE LOVE my apron! Last night I wore it, just to watch tv with my husband. :)
Oddly enough, it is the exact pattern that I wanted to make for my partner, but I was too scared that I wouldn't be able to pull it off.
Thank you. And thank you for the potholder and all the goodies.
My little girl was so excited that you remembered her!
I'll try to blog about it early next week.
Thanks again!
- September 11, 2008 at 4:18 PM
- micki said...
heehee you sound like me. delinquent in mailing. it's a chronic problem.
- September 12, 2008 at 5:37 PM
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Christmas Pudding
I'm a bit late this year with the Christmas Puds but here's the recipe I always use.
4 oz shredded veggy suet
2 oz self raising flour
4 oz breadcrumbs
1 tsp mixed spice,
1/2 tsp each of cinnamon and grated nutmeg
Grated rind and juice of a lemon
Grated rind of an orange
8oz soft brown sugar (muscovado)
14 oz of sultanas, currants and raisins - in a mix that pleases you.
1 oz of candied peel, chopped
1 oz ground almonds
1 bramley apple, chopped small
5 fl oz of guinness or similar stout
2 large eggs
Measure all the ingredients into a bowl and mix. Cover and leave overnight. This makes 1 large pudding but you can divide into 2 smaller ones - adjust the steaming times - and make sure you fill the bowls nearly to the top. Grease the bowls with butter and cover with greaseproof paper and foil before cooking.
Steam or boil (put a saucer or similar in the bottom of the pan so it takes the bowl off the base). Keep the pan filled with boiling water during cooking (it should come to about half way up the bowl) Steam for 4 hours for small puddings and 6 for a large one. Allow to cool and wrap in clean paper. On the day of eating, steam again for about 1/2 hours to heat through.
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