In dieser neuen Sektion bringen wir neueste bio-wissenschaftliche Ergebnisse

und Vermutungen. Zuerst auf Fach-Englisch und dann auch für die breite Leserschaft.

 

Die Pandemie hat Menschen bereits zu rasanten Fortschritten vor allem bei den Impfstoffen angespornt.

Ähnliches wünschen wir uns auch zur besseren Bewältigung der Depressionen.

 

Dans cette nouvelle séction nous vous apportons les derniers résultats et hypothèses

bio-scientifiques. Ceci d'abord en anglais d'experts et ensuite aussi pour le grand public.

La pandémie a déjá conduit les humains à des progrés rapides notamment pour les vaccins.

Nous nous souhaitons le même pour une meilleure maîtrise des dépressions.

 

In questa sezione nuova v´apportiamo gli ultimi risultati ed ipotesi dalle bio-scienze. Dapprima in inglese da specialisti e poi anche per l'ampio pubblico.

La pandemia ha già stimolato gli umani verso rapidi progressi, soprattutto nei vaccini (Fauci).

Ci auguriamo progressi simili per affrontare meglio la depressione.

 

 

Inhalte / Contenus / Contenuti / Contents

 

1a. ENERGIE-GELADEN GEGEN DEPRESSIONEN. (clic!) 1b. Mutter nach KIndsmisshandlung, Epigenetik nur beim Neugeborenen gesund, PNAS oct 2020.

- Alexander Karabatsiakis, EDA-Repräsentant für Österreich.

2. Biology trends in Depression 2020: THE TREMENDOUS CHALLENGE of Covid-19.

- Gottfried R. S. Treviranus, EDA-Repräsentant für die Schweiz.

 

 

Biology trends in Depression 2020:

 

THE TREMENDOUS CHALLENGE of Covid-19.

Gottfried R. S. Treviranus, Berne

 

The humans are still beeing tremendously challenged by the pandemic even in some of the relatively spared high-consuming, well-equipped societies, which revealed unsuspected voids of resilience and an escalation of disparities. The toll among frontline (para-)medics has been appalling, shattering trust in recent sanitary policies. All this in the humans triggers strong emotional reactions, but not necessarily depressions, which are illnesses, probably even more often grafted on already previous «affective» temperaments, than dire consequences of noxious stress by themselves.1 The roads to depression from the pandemic obviously are many, and those via deteriorating medical, anti-infectious, and mental care can be predicted to be as important as those from exhausting psycho-social worry and despair. Here we focus on the possible direct tracks from Covid-19 to depression.

 

Only 3% of the initial published scientific output on the medical issues of the COVID-19 pandemic concerned the damages to mental health,2 as an account from the U.S.A. mirroring the effects during the early phase in a way representing the overall population now remarks.3 An even more minute proportion covers observations of putative mechanisms involved in the specific biological contribution to the depressive and other loads burdening human mental health.

 

Here we try to catch a glimpse of first insights most directly related to biological issues of depression from Covid-19, the equally dangerous SARS and MERS, and from what is known about the other coronavirus affecting the CNS of humans (HCovs) like the four others causing one in three common colds.4 Researchers now zoomed in on weaknesses of human defence against Covid-19, and notably on the natural immune responses` interferon-type1-systems either through genetical variants in 4%5 or through anti-INFg-antibodies, a mechanism known from Mycobacteria, Staphylococcus, and Candida,6 all subverting immune cells by colonization, which again may be central to neuropsychiatric disorders as far as related to mast cells and arteries.7

 

The astonishing skills in subverting bodily (and mental) functions of the COVID-19 virus, which is a member of this increasingly infamous group of 7 human viruses, are encoded in an encapsulated huge single strand of RNA. These skills rapidly spurned theories on usurpation of physiological, particularily immune networks8, mast cell involvement,9 cerebral auto-immunity, the origin of age- and sex-correlations, the arterial aneurysms creation, the role of antibodies favoring receptor and clathrin-facilitated entry, the pharmacodynamics of the few testable drugs, the peculiarities of the young either protected or not, and many more.10

 

How Covid-19 might enter proper CNS-tissues

 

Broad neurological symptoms in a quarter of Covid-19-illnesses are proportional to overall severity, comorbidity, and age, but may also devastate children. As far as these many and variagate neuropsychiatric disturbances and lesions to the CNS are concerned, the modes of entry of theses virus into the brain through its barriers and into its proper tissue cells are approached via tentative models. General cell entry requires the ACE2-receptor, which again interacts with TMPrSS211 - both effectively blocked by drugs12 -and neuropilin-113, and it its followed by clathrin-mediated endocytosis – blockable by cheap and common phenothiazines14,15,16 among other useful psychotropics like lithium17 or clomipramine18 - and replication with lysosomes participating,19 one of the places hydroxychloroquine acts.20

Some CoV can enter the neurons – were they rush to the endoplasmatic reticulum of cells21 or may persist22 - via peripheral nerves crossing synapses or via the neural olfactory bulb above the ethmoïd cells. A review from Thessaloniki23 next to the nerval routes and hematogenous spread mentions «nasal epithelium in general» and «lymphatic tissue». In fact air pollution particles reaching the nose can function as vectors carrying Covid-19 too.24 While Covid-19 is assumed to be carried in the blood stream especially of arteries and arterioles, special complex and variegate barriers made up of many other cells protect the neural tissues. Covid-19 has been erroneously identified25 within arterial endothel (what the same institution which fallaciously smeared26 the use by front-line doctors of hydroxy-chloroquine27 denies)28 - which would have expalined the proven replicatory invasion of an endothelial organoid,29 particularly enlightening, as no immunocyte contribution war required. Autopsy finding instead showed their dense perivascualr presence, and a much incrased angiogenesis and microthrombotic activity.30 That Covid-19 could colonize macrophages, which thereafter would spread these «trojan horses» was observed,31 but not extended to brain parenchyma invasion, which normally is not achieved by them,32 but instead by mast cells,33,34 which can be colonized by many germs or viruses,35 and are also required for CNS-autoimmunity.36

 

 

This article will be complemented over the next days.

 

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2EppiCentre Social Science Research Unit, COVID-19: A living systematic map of the evidence. (Accessed July 22, 2020). [http://eppi.ioe.ac.uk/cms/Projects/DepartmentofHealthandSocialCare/Publishedreviews/

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12Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen S, Schiergens TS, Herrler G, Wu NH, Nitsche A, Müller MA, Drosten C, Pöhlmann S. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell. 2020 Apr 16;181(2):271-280.e8. doi: 10.1016/j.cell.2020.02.052. Epub 2020 Mar 5. PMID: 32142651; PMCID: PMC7102627.

13Davies J, Randeva HS, Chatha K, Hall M, Spandidos DA, Karteris E, Kyrou I. Neuropilin‑1 as a new potential SARS‑CoV‑2 infection mediator implicated in the neurologic features and central nervous system involvement of COVID‑19. Mol Med Rep. 2020 Nov;22(5):4221-4226. doi: 10.3892/mmr.2020.11510.

14Otręba M, Kośmider L, Rzepecka-Stojko A. Antiviral activity of chlorpromazine, fluphenazine, perphenazine, prochlorperazine, and thioridazine towards RNA-viruses. A review. Eur J Pharmacol. 2020 Sep 16;887:173553. doi: 10.1016/j.ejphar.2020.173553. Epub ahead of print. PMID: 32949606; PMCID: PMC7493736.

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17Sato SB, Taguchi T, Yamashina S, Toyama S. Wortmannin and Li+ specifically inhibit clathrin-independent endocytic internalization of bulk fluid. J Biochem. 1996 May;119(5):887-97. doi: 10.1093/oxfordjournals.jbchem.a021326. PMID: 8797088.

18Javelot H, Weiner L, Petrignet J, Meyer G, Briet J, El-Hage W, Hingray C. Psychoactive compounds as multifactorial protection factors against COVID-19. Ir J Med Sci. 2020 Aug 18:1–2. doi: 10.1007/s11845-020-02346-9. Epub ahead of print. PMID: 32812114; PMCID: PMC7433988.

19Amini Pouya M, Afshani SM, Maghsoudi AS, Hassani S, Mirnia K. Classification of the present pharmaceutical agents based on the possible effective mechanism on the COVID-19 infection. Daru. 2020 Jul 30:1–20. doi: 10.1007/s40199-020-00359-4. Epub ahead of print. PMID: 32734518; PMCID: PMC7391927.

20Shukla AM, Archibald LK, Wagle Shukla A, Mehta HJ, Cherabuddi K. Chloroquine and hydroxychloroquine in the context of COVID-19. Drugs Context. 2020 Apr 28;9:2020-4-5. doi: 10.7573/dic.2020-4-5.

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35 Treviranus GRS. Psychoses by attacks from subverted mast cells: a role for arterial intramural flow badly steered by the nasal ganglia? Psychiatria Danubina, 2020 32, S2: 239–64.

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