Hi friends!

 

Today is a beautiful day in Stockholm with blue sky. However, I had a headache yesterday which unfortunately has continued today. Measured my blood pressure which is to high, both of them. Two months ago I started to wear lenses, maybe that is the problem. I will go back to wear glasses. So I have to stay at home and rest in peace. Talked to my parents  and they are making cinnamon rolls today. Lady and Tippa are both fine. If I get better I will make some apple (from the countryside) muffins later. So today is a lazy day. Hope I get better so I can go to work tomorrow.

Almost a year has passed since I wrote my very first poem and that was at halloween 2012. This website is supposed to give me energy. I actually re-read what I have written some times. My diary.

Have nice day!

Anna

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Since I am not directly involved in science I will instead present theoretical science. This is not something that is finished this year. I will make some small changes and because I don´t have access to anything but my memory I will build research from my memory. Grammar etcetera may not be right.

This is very difficult, I can assure, but challenging.

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“Je pense, donc je suis”

Descartes

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I have thought for quite same time; and these are my working hypotheses:

1) Dopamine and -acetylcholine hypothesis

Smoking (or other forms of nicotine intake) is very common in several diseases. Professor Arvid Carlsson (Göteborgs Universitet, Sweden) has hypothesised in the 1950’s that dopamine is involved in the pathophysiology of eg addiction (Engel and Söderpalm 1999; Yoshida et al 1980), schizophrenia and Parkinson´s disease. (don´t know about Alzheimers disease). Smoking is highly observed among alcohol dependent individuals, depression, schizophrenia.

Several experiments in vivo have demonstrated that dopamine plays a crucial role in these diseases. Professor Arvid Carlsson has further gained evidence for the hypothesis by introducing dopamine stabilisers. A pharmacological substance, with dual effects, acting as an agonist and antagonist depending on the state of the environment. (Since I write this from my memory, it may not be accurate).

However, as seen in Parkinson´s disease, today´s available pharmacological treatment is not optimal. On-off symptoms may be observed.

Dopamine neurons are widely distributed throughout the brain in rather distinct pathways. These neurons are closely located to eg cholinergic neurons. Cholinergic neurons have muscarinic (G-protein coupled) and nicotinic receptors (ion channels). To the best of my knowledge, dopamine neurons do not have ionic receptors. Maybe they are equipped with rapidly responding receptors, but they have not been found or simply: they do not exist. I don´t know the literature.

Inte helt lätt att hålla röda tråden…Men det är ett andra utkast.

A possible way to reduce side-effects may be to give more input to dopaminergic activity by cholinergic sparkling eg from the mesopontine area.

Since I have experienced that data can be stolen I publish this in public so everybody can get the information. It might be wrong but that is what a hypothesis may be. Probably it is right but it may also be wrong. Or something in-between. Only experiments can find out to get evidence for the hypothesis to help individuals with proper treatment.

Hopefully I can help people. Maybe somebody will read this and get ethical approval.

 

2) Prevention of diseases in humans later in life is to monitor ophthalmological status in newborns – to obtain stability in the body

Since I have read a lot about the brain in the literature a decade ago I have had time to reflect. It is interesting to note that the

I believe (a hypothesis that might be wrong) that the development of the ophthalmological nervous system is very important for the brain, our function to be. Both “eyes” need to be in balance during development. However, since the brain is adaptable to changes, can later be corrected, and balance can be re-obtained.

These are just, so far some ideas, so they are not true.

3) Is it possible to predict depression by monitoring cortisol levels, and can beta-blockers (not crossing the blood-brain barrier, “heart-selective”, eg metoprolol) together with SSRI (sertralin) contribute to a rapid recovery and hampering of ?

Jag undrar om depression kan på något sätt försämra hjärnans funktion, alltså, utan depression är hjärnan ok, men en hjärna som varit med om en depression kan sensitiseras och därmed vara känsligare i framtiden. Det skulle eventuellt, den mycket välkända beta-blockeraren metoprolol hjälpa till att lindra. En låg dos kanske 25 mg dagligen.

Om så är fallet, skulle det med en redan väl beprövad beta-blockerare kunna

These questions need to be further explained, I have not fully formulated good questions and thoughts.

 

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