The eight mechanisms of anti-Alzheimer’s effects of curcumin

Related: Resveratrol and curcumin, plant’s own weapons that protect the brain

1. Curcumin is a better antioxidant than alpha-tocopherol and can protect blood vessel cells from oxidative stress caused by Amyloid beta peptide (Abeta), the main constituent of amyloid plaques in the brains of Alzheimer’s disease (AD) patients. Interestingly, with low-dose curcumin, but not with high-dose curcumin the plaque occurrence was decreased by up to 50%.

2. Curcumin significantly lowered levels of oxidized proteins, which content is elevated in the brains of mice model of AD.

3. Curcumin inhibits the formation of fibrillar Abeta (fAbeta) and destabilized already formed fAbeta.

4. In animal models of AD, curcumin prevented cognitive deficits presumably by binding the redox-active metals Fe and Cu.

5. Curcumin decreased Abeta formation. When fed to aged mice with advanced amyloid accumulation, curcumin directly binds small beta-amyloid and blocks fibril formation.

6. Beta-amyloid peptide can form a peroxidase playing a major role in the pathologies of AD. Curcumin inhibits this peroxidase.

7. Curcumin enhances the phagocytosis and Abeta removal by macrophages, the process that is impaired in patients with AD.

8. Curcumin crosses the blood–brain barrier, disrupts existing plaques and partially restores damaged neurones in annimal AD model leading to a significant reversal of structural neuronal damage.

Source

B.B. Aggarwal, K.B. Harikumar. Potential therapeutic effects of curcumin, the anti-inflammatory agent, against neurodegenerative, cardiovascular, pulmonary, metabolic, autoimmune and neoplastic diseases. The International Journal of Biochemistry & Cell Biology 41 (2009) 40–59

Cannabinoids, marijuana – health effects

Question: Hi. Please, before you claim this as outside of your expertise I would really appreciate your answer even if it is only a little information, you can send it to my email privately at too if you wish. So, I was wondering, what does marijuana do to our bodies and brains? How dangerous can it be?

I’m only asking because i smoked for 2 years then stopped for 3, and now I am doing it for a few weeks, not for recreational reasons though. And when I did it a few days ago my heart was pounding like crazy, I felt like I was going to die and I was thinking some crazy thoughts, and so I’m just trying to make sure i’ll be safe if I continue for the next few weeks?

I’m 19 and male. Thank you.

Answer: Dear Josh,

I’m listing the major known negative reactions caused by marijuana. Since I know neither the purpose of your return to marijuana nor your overall health condition, you must draw your own conclusions. Please don’t hesitate asking me any further questions especially if you find my reply too technical.

The plant Cannabis sativa has been used for or medical and religious purposes for at least over 4000 years and has been globally adopted for recreational use for the past 50 years. It’s been estimated that 166 million adults aged 15–64 years currently use cannabis. The psychoactive chemical of cannabis is Δ-9-tetrahydrocannabinol (THC). The deadly dose of THC is between 15 g and 70 g — much higher than that can be smoked by even a heavy user.

The most common acute negative reactions are frequent in beginning users. They are: anxiety, panic reactions including tachycardia (fast heart beat), and psychotic symptoms. Chronic users can suffer from memory deficits, motor performance impairment; as a result, cannabis users had higher rates of hospital admission for injury from all causes although alcohol intake has greater impact: driving after having taken cannabis increases the risk of vehicle crashes 2–3 times compared with 6–15 times under the influence of alcohol.

Other adverse effects include decreased levels of testosterone and increased rates of birth defects in babies born to mothers taken cannabis during pregnancy.

The lifetime risk of dependence in cannabis users is about 9% comparing with 32% for nicotine, 23% for heroin, 17% for cocaine, 15% for alcohol, and 11% for stimulant users.

Cannabis smoke contains many of the same carcinogens as does tobacco smoke so it’s no surprise that case–control study of hospital-diagnosed lung cancer and community controls indicated an increased incidence of lung cancer in cannabis users even after adjustment for cigarette smoking.

Cannabis use changes brain functions that can be detected by modern methods like positron emission tomography, and electroencephalography. Among most reproducible effects of cannabis withdrawal are: lower brain blood flow in certain regions of brain  cortex,  less activity in brain regions involved in memory and attention and changes in cannabinoid receptor activity in the hippocampus, prefrontal cortex, and cerebellum.

Tanya Zilberter

Source

W Hall, L Degenhardt. Adverse health effects of non-medical cannabis use. Lancet 2009; 374: 1383–91

Mirror neurons, autism, and the theory of mind

Related: Schrödinger’s One Mind :: Non-local mind bibliography

The theory of mind presumes that we can only imagine that others have a mind because we have no direct access to the mind of another. In the late 1980s, this theory seemed to be fortified by experimental data describing a population of brain cells (named by researchers “mirror neurons”) – becoming active when a monkey watched another animal act – where first described.

Mirror neurons or, in humans, mirror brain areas, are those that act similarly whether a subject of experiment perform an action or sees how the same act is performed by another being. Recently, the experiments were extended to analyze emphatic reactions (Seeing someone is in pain, seeing the faces of people in pain, seeing hands or feet in painful situations). Click to see the picture 1 and picture 2.

The enthusiasts see in these facts many hopes: to pinpoint in the brain’s hardware the processes of understanding, altruism, decision making, to finally grasp what’s wrong in the brain of the autistic, etc. The skeptics call for stricter analysis and interpretation. The major problem with mirror neurons, they say are: the lack of evidence that these neurons relate, as implicated, to understanding or language, different anatomical representation in monkeys and humans and between understanding and acting in both, and some other discrepancies that are very technical.

Sources

C Keysers, JH. Kaas, V Gazzola. Somatosensation in social perception. Nature Reviews Neuroscience, v 11, 2010: 417

talkingbrains.org

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