Anandamide is an endogenous (meaning developed from within, naturally occuring) cannabinoid neurotransmitter. The name is taken from the Sanskrit word ananda, which means bliss or delight. It is synthesized from N-arachidonoyl phosphatidylethanolamine by multiple pathways. Its is degraded primarily by the fatty acid amide hydrolase (FAAH) enzyme, which convers ananda into ethanolamine and arachidonic acid. Inhibitors of FAAH lead to elevated anandamide levels and are being persued for therapeutic use.
A neurotransmitter in the brain and local chemical messenger outside of the brain, dopamine has various different effects in the body
Dopamine plays a big role in reward-motivated behavior which is exhibited by an increase in dopamine levels in the brain.
Many drugs, such cocaine, amphetamines, and methamphetamine work by amplifying the effects of dopamine, a characteristic that researchers theorize makes them so addicting.
Dysfunction of the dopamine system is responsible for many diseases such as Parkinson’s and potentially schizophrenia, ADHD, and restless leg syndrome.
In addition to the reward system, dopamine also has important roles in motor control, motivation, arousal, lactation, and sexual gratification.
Outside of the brain, dopamine has a repressive effect on tissues of the immune system, specifically lymphocytes. Currently, this is being studied to find the link between the nervous system and immune system and dopamine’s potential role in autoimmune disorders.
Dopamine is an important precursor for the synthesis of two other neurotransmitters; epinephrine and norepinephrine
There is a neurotransmitter called adenosine, this neurotransmitter produces sleepiness. It accumulates throughout the day and declines during sleep. So your adenosine levels are at its highest before you go to sleep.
Caffeine looks a lot like adenosine. So when caffeine enters the body, it binds to the receptor sites designed for adenosine. Therefore, even though your adenosine levels are rising, they are not binding to its receptor sites, because caffeine is already chilling there. So you will be more awake. :)
If caffeine does not affect you very much, it could mean that you do not have as many adenosine receptor sites as other people.
An immunosuppressive drug could delay the onset of neurodegenerative diseases
Rapamycin, a drug used to prevent rejection in transplants, could delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s. This is the main conclusion of a study published in the Nature in which has collaborated the researcher Isidro Ferrer, head of the group of Neuropathology at the Bellvitge Biomedical Research Institute (IDIBELL) and the Bellvitge University Hospital and Full Professor of Pathological Anatomy at the University of Barcelona. The research was led by researchers from the International School for Advanced Studies (SISSA) in Trieste (Italy).
The collaboration of the research group led by Dr. Ferrer with SISSA researchers began five years ago when they observed that Parkinson’s patients showed a deficit in UCHL1 protein. At that time, researchers didn’t know what mechanism produced this deficit. To discover it a European project was launched. It was coordinated by the Italian researchers and participated by other European research groups, including the group led by Dr. Ferrer. The project, called Dopaminet, focused on how dopaminergic neurons (brain cells whose neurotransmitter is dopamine) are involved in Parkinson’s disease.
Contrary to most common hypothesis that a DNA fragment encodes a protein through a messenger RNA molecule, the researchers found that it also works in reverse. They found a balance between the protein and its mirror protein, which is configured in reverse, and they are mutually controlled. If the protein mirror is located in the nucleus of the cell, it does not interact with the protein, while if it is in the cytoplasm, then both of them interact.
In the case of Parkinson’s disease the protein UCHL1 appears reduced and also its mirror protein is localized in the nucleus, and in the cytoplasm. Thus, the researchers sought a method to extract the mirror protein from the nucleus and made it interact with the original UCHL1 protein. The authors found that rapamycin was able to extract them from the nucleus. The drug allows the two proteins, the UCHL1 and its mirror, hold together in the cytoplasm, which would correct the mistakes that occur in Parkinson’s disease.
This in vitro research has allowed describing a new unknown mechanism. It is necessary that the UCHL1 mirror protein should accumulate in the nucleus and escape from the cytoplasm and join the UCLH1 protein. The combination of both makes the system work.
“The rapamycin can not cure Parkinson’s disease, but it may delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s itself. Rapamycin can protect and delay the beginning of these diseases. It can complete the treatment, but it should be combined with other existing treatments”, explains Isidro Ferrer.
Anyway, it is still far its application in patients. The next step is to validate these results in animal models and study the effects of rapamycin in combination with other drugs.