https://www.europesays.com/it/733994/ Grande Fratello Vip, Andreas Muller rifiuta di ballare con Megan Ria. Ilary Blasi: «Sii più aperto, non è carino questo rifiuto» #AndreasMuller #Entertainment #GrandeFratelloVip #IlaryBlasi #Intrattenimento #IT #Italia #Italy #MeganRia
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51 results for “AndreasM”
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Tim Fehlbaum – „Hell“ (2011)Das Ende der Welt hat wahrscheinlich selten so geblendet. Denn in dieser SciFi-Dystopie brennt die Sonne mit apokalyptischer Präzision alles weg, was an Zivilisation erinnert – sozusagen als als ökologischer Rückstoß. Tim Fehlbaum verzichtet in seinem Spielfilmdebüt (produziert von Roland Emmerich) auf Aliens, Tsunamis, Asteroiden und die ganz große Effektschlacht. Stattdessen herrscht gleißendes Weiß in einer ausgetrockteten Welt ohne Schatten und ohne Gnade in einer Near-Future-Version von Deutschland. Mit Hannah Herzsprung, Lars Eidinger, Lisa Vicari und Stipe Erceg. (ZDF, Wh.)
Zum Blog: https://nexxtpress.de/mediathekperlen/tim-fehlbaum-hell-2011/ -
Hello Mastodon! I'm Andreas, looking forward to meeting you.
I lead Professional Services at Elsevier, where I focus on innovative ways of looking at scientific data in the life sciences. Ex-AWS, Ex-Sanofi. Customer focused, always.
I love playing D&D, noodling around with my guitar(s), reading comics and novels, and starting more side projects than I could ever finish. I love learning about new coding projects, I have started too many blogs, and I'm trying to be optimistic about the future my kids will inherit.
Looking forward to meeting folks here.
#TTRPG #LifeScience #Bioinformatics #Introduction #introductions #Boston #DedhamMa
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USA, i latinos alle elezioni di midterm
di Dan La Botz Gli ispanici, i cui voti hanno contribuito alla vittoria di Trump nel 2024, si stanno allontanando da lui a causa dell'alto costo della vita e degli sfratti violenti. La loro rabbia potrebbe costare ai repubblicani la maggioranza al Congresso. […]https://andream94.wordpress.com/2026/10/18/usa-latinos-midterm/
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Trump, in guerra per debolezza
Il suicidio della superpotenza USA in Iran e in Russia di Timothy Snyder, da Substack Timothy Snyder Conosciamo la frase "pace attraverso la forza". La sua logica è evidente. Un paese forte può dissuadere gli altri dal fare la guerra. Un paese forte può sostenere la ricostruzione dopo un conflitto. Un paese forte attrae alleati e costruisce relazioni. Se necessario, un paese forte può vincere una guerra. Sotto Donald Trump, gli Stati Uniti non sono un paese forte in nessuno di questi sensi, né in alcun senso in generale. Al contrario, sono un paese che genera e prolunga la guerra a causa della propria debolezza. […]https://andream94.wordpress.com/2026/10/18/trump-in-guerra-per-debolezza/
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Sentinel • Lamella • A single architectural gesture — the vertical facade rib — seen three times: soaring, inhabited, abstracted. • Kassel • Hesse • Germany #alternatiffotograf #andreaslbergphotography #Architecture #Architektur #art #artist #blackandwhite #bw #bwphotography #contemporaryart #dynamic #fineart #fineartzone #fotografie #germany #Hesse #kassel #kasselcity #Lamella #photography #schwarzweiss #sharp #street #streetphotography https://www.andreas-l-berg.com/blog/sentinel/
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L’asse Trump-Putin sempre più evidente
da Against The Current Ciò che era evidente a molti osservatori fin dall'inizio della seconda presidenza di Donald Trump è ora venuto clamorosamente alla luce: Donald Trump e Vladimir Putin sono alleati nella guerra della Russia per mutilare e soggiogare l'Ucraina. Cosa ci guadagnano entrambi da questa alleanza da gangster? […]https://andream94.wordpress.com/2026/10/17/lasse-trump-putin-sempre-piu-evidente/
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Israele divisa verso il voto ma senza prospettive di cambiamento
di Avrum Burg, deputato israeliano, ex laburista e ex presidente del parlamento israeliano, ora eletto nelle fila della formazione antisionista Hadash, da The Observer Apochi giorni dalle elezioni, Israele è una pentola a pressione, con ogni candidato che alza la fiamma. Uomini ultraortodossi si ribellano per impedire alla polizia militare di arrestare i renitenti alla leva. Coloni estremisti attaccano le comunità palestinesi in Cisgiordania con brutale violenza. La criminalità violenta imperversa nelle città arabe mentre lo stato resta inerte. Le famiglie delle vittime del 7 ottobre continuano a chiedere giustizia. I dati su depressione, traumi e suicidi sono allarmanti. L'emigrazione e il crollo della fiducia nelle istituzioni pubbliche non hanno precedenti. […]https://andream94.wordpress.com/2026/10/17/israele-divisa-verso-il-voto/
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Brasile, la campagna per il ballottaggio tra orario di lavoro e corruzione
E' stata approvata la riduzione dell'orario di lavoro con 75 voti favorevoli e 1 contrario; un sondaggio Datafolha mostra un "pareggio tecnico" tra Lula e Flávio Bolsonaro; il Tribunale Superiore Elettorale (TSE) impone la parità di trattamento tra Meta (la società di Facebook) nella campagna elettorale, mentre le accuse contro Daniel Vorcaro continuano ad alimentare lo scontro politico. (nella foto in alto, alcuni parlamentari del PSOL al momento dell'approvazione definitiva della riduzione di orario di lavoro) da Revista Movimento […]https://andream94.wordpress.com/2026/10/17/brasile-orario-e-corruzione/
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Russia, una sanguinosa transizione verso un nuovo vecchio imperialismo
Alcuni giorni fa, segnalandone la pubblicazione in inglese, abbiamo riprodotto l'introduzione al volume Russia's New Imperialism: Capital and Ideology (Il nuovo imperialismo russo: capitale e ideologia, Stanford University Press, 2026), opera di due autori noti alle lettrici e ai lettori del Refrattario: Ilya Budraitskis (attivista marxista russo) e Ilya Matveev (caporedattore di Posle.Media). Qui sotto pubblichiamo la recensione del libro scritta da Simon Pirani, ripresa da links.org.au […] -
Andreas Schmitz: "Ich dachte, meine Wärmepumpe wäre SPARSAM – dann kam DAS 10€-Teil! MEGA!"
https://www.youtube.com/watch?v=5lLhnls90f0
#SonnenEnergie #Wärmepumpe #Akkudoktor #AndreasSchmitz #Heizung #Energiekosten
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Al #GrandeFratelloVip, Andreas Müller non accetta la sfida di ballo con Megan Ria proposta da Ilary Blasi. Il rifiuto apre un confronto sul loro rapporto nella Casa e sul legame complicato che il concorrente racconta di avere con la danza.
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Häkelfiguren im „Flauschfach“ sorgen am Bielefelder Nordpark für Freude | Nachrichten aus Ostwestfalen-Lippe
© Andreas Zobe „Do it yo…
#Bielefeld #Deutschland #Deutsch #DE #Schlagzeilen #Headlines #Nachrichten #News #Europe #Europa #EU #CarolinNeumann #Familie #Flauschfach #Germany #Instagram #label_foto #label_inspirieremich #label_xl160 #meta_eo_zusammenfassung #meta_userneeds_inspirieremich #Nordpark #Nordrhein-Westfalen #PayPal #Selbstbedienungsschrank
https://www.europesays.com/de/1352945/ -
Friede und Grüße ins Fediverse!
Hier ist der Andreas und ich bin Anarchist, der im Herzen immer Monarchist war. Ich mag Widersprüche und liebe es sie zu erkunden. Brotfresser wurde ich schon als Kind genannt, weil ich ein kleiner Klugscheißer war. Ich suche: menschliches Gegenüber, in allen seinen Facetten und Widersprüchlichkeiten. Vielleicht Gemeinschaft und gemeinsame Projekte. Austausch über Gott und die Welt.
#Philosophie #Geschichte #Pädagogik #Bildung #Technik #Glaube #Kultur #Literatur -
Drygt fem veckor efter valnatten saknar Sverige fortfarande en regering. I eftermiddag ska riksdagens talman Andreas Norlén hålla pressträff om hur landet ligger.#centerpartiet #miljöpartiet #vänsterpartiet
Vad blir nästa steg i regeringsbildningen? -
La proposta di Ilary Blasi di organizzare una sfida di danza al GF Vip si ferma davanti al rifiuto di Andreas Muller. Il confronto con Megan Ria prosegue tra critiche delle opinioniste e nuove tensioni dopo la diretta. #GrandeFratelloVip
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📰 "Le pedía un último abrazo": Pancha Merino reveló detalles de su quiebre con Andrea Marocchino
🔗 https://www.biobiochile.cl/noticias/dopamina/2026/10/16/le-pedia-un-ultimo-abrazo-pancha-merino-revelo-detalles-de-su-quiebre-con-andrea-marocchino.shtml -
✅️ PRÜFbericht Nr. 2/2026:
Freitag im Bundesrat: MV-Ministerpräsidentin Manuela Schwesig spricht sich für eine verfassungsrechtliche Prüfung der AfD aus. Bundesratspräsident Andreas Bovenschulte fordert eine Bund-Länder-Arbeitsgruppe. [https://www.bundesrat.de/SharedDocs/pm/2026/25_bilanzrede_bovenschulte.html]
🧐 #pruef_facts: „Prüfen heißt nicht verbieten. Prüfen heißt, unsere Pflicht zu erfüllen.“ Entscheiden kann allein Karlsruhe.
Ordnung muss sein!
#pruef #pruef_be #OrdnungMussSein #bundesrat #demokratie #grundgesetz #wehrhaftedemokratie -
In #Berlin kam es am Freitag, dem letzten Schultag vor den Ferien, vor dem Andreas-Gymnasium im Bezirk #Friedrichshain zu Protesten. Ab 7:30 Uhr hatten etwa 100 Schüler*innen den Vorder- und Hintereingang blockiert. Nach Angaben der Initiative #Schulstreik gegen Wehrpflicht ging es dabei vor allem gegen die Wiedereinführung der #Wehrpflicht sowie Forderungen nach mehr Geld für Bildung.
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Schülerproteste in Berlin: Was sind die Forderungen? - YouTube
https://www.youtube.com/watch?v=BivSqYlcieg
Vor dem Andreas-Gymnasium in
#Berlin-Friedrichshain gab es am Freitag
#Proteste von Schülern und Schülerinnen - auch schulfremde Personen waren...
#jakobsweg
#caminodesantiago
#buencamino
Schülerproteste in Berlin: Wa... -
Für ein Buch, dass ich schon vor einer Weile durchgelesen habe, habe ich nun meinen Blogartikel fertig:
„Pride Began on Christopher Street“ von Christian Handel und Andreas Suchanek, ein schnulziger historischer Feel-Good-Roman mit positivem Ende.
https://blog.varb.in/pride-began-on-christopher-street-von-christian-handel-und-andreas-suchanek/
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#Sauerteig #Brotbacken #Zuhause #athome
Mit niedrigtemperatur Hefen, bei 160°C gebacken. #Vollkorn #Roggen #Weizen Mischbrot. Mahlhgrad 2 auf der Havos Queen 1. Rezept nach Andreas Sommers (YT) -
Forscher: Meeresboden bremst Eisschmelze in Antarktis
Das Team des deutschen Forschungsschiffes "Polarstern" hat vor der Ostantarktis entdeckt: Der Meeresboden hilft dabei, das Schmelzen des Eises dort zu bremsen. Von Andreas Kegel.
#Antarktis #Eisschmelze #"Polarstern"
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https://www.europesays.com/it/733886/ Grande Fratello Vip: Moreno Morello eliminato, in gara Andreas Müller, Giacomo Gallani, Jonathan Kashanian, Marina La Rosa e Megan Ria #Canale5 #casa #Entertainment #GrandeFratelloVip #IlaryBlasi #Intrattenimento #IT #Italia #Italy #MorenoMorello #Televoto #tv
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🏫 Welchen Beitrag können Schulen zur Stärkung demokratischer Kultur und zum gesellschaftlichen Zusammenhalt leisten? Zu dieser Frage haben sich Vertreterinnen und Vertreter u.a. aus Schulen, Politik und Wissenschaft in Stuttgart beim Landestreffen „Schule ohne Rassismus – Schule mit Courage“ ausgetauscht.
🗣️ Kultus-Staatssekretär Andreas Deuschle MdL betonte bei seinem Impulsvortrag: „Sich für Vielfalt und Menschenwürde einzusetzen, war noch nie so wichtig wie heute! Das Netzwerk ‚Schule ohne Rassismus – Schule mit Courage' steht genau für diese Werte ein. In Baden-Württemberg haben wir im Bereich der Demokratiebildung eine große Expertise, eine starke Trägerlandschaft und vor allem eine hervorragende Zusammenarbeit. Dafür möchte ich allen Beteiligten danken, ebenso wie den Lehrkräften und Schulleitungen, die sich mit großem Engagement dafür einsetzen, dass ‚Schule ohne Rassismus‘ kein bloßes Label an der Schulpforte ist, sondern im Alltag von Schule und Unterricht durch viele Ideen, Aktivitäten und vor allem mit Haltung gelebt wird.“
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Cloppenburg: AfD-Kandidat lehnt versehentlich seine eigene Wahl ab - DER SPIEGEL
> »Ich ärgere mich gewaltig«: Weil er auf einem Formular das Kreuz an der falschen Stelle setzte, verlor Kandidat Andreas Bluhm den sicheren Sitz.
Muahhhahhahhaaaaahhhhaaahhhaaaahhhhhaaaah 😂😂😂
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DATE: October 17, 2026 at 08:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Scientists identify DNA regions tied to binge eating, including one near a well-known obesity gene
A large genetic analysis has identified DNA regions linked to binge-eating behavior and anorexia nervosa, suggesting that the two share genetic ties to other psychiatric conditions but run in opposite directions when it comes to body weight. The findings, published in Nature Mental Health, extend eating disorder genetics beyond its long focus on anorexia.
Anorexia nervosa is a condition where individuals experience an intense fear of gaining weight, leading them to severely restrict their food intake to maintain a dangerously low body weight. Binge-eating behavior involves episodes of eating unusually large amounts of food while feeling a loss of control.
Eating disorders also overlap, and people often move from one diagnosis to another over time. A 2010 twin study found that anorexia and bulimia nervosa, a condition in which people of normal or higher weight binge eat and then try to compensate through behaviors such as vomiting or fasting, share a moderate portion of their genetic risk. Large-scale gene-mapping studies, however, have centered on anorexia: a 2019 study by the same research consortium identified the first eight genetic regions linked to the disorder, and its authors argued that anorexia has both psychiatric and metabolic roots.
Binge eating has received far less genetic attention, even though it appears across several eating disorders. A 2021 study by members of the same network found that people with binge-type eating disorders tended to carry more genetic variants linked to higher body mass index (BMI), a measure of weight relative to height, pointing to the need to map binge eating’s genetics directly.
The new study was led by Jet D. Termorshuizen of Karolinska Institutet and Helena L. Davies and Sang-Hyuck Lee of King’s College London, who contributed equally, with Jonathan Coleman, a senior lecturer in statistical genetics at King’s College London, among its senior authors. The work was carried out by the Eating Disorders Working Group of the Psychiatric Genomics Consortium, an international research collaboration.
“We had previously carried out a large genetic study of anorexia nervosa and we wanted to expand this and implicate more regions of the genome as associated with this disorder,” Coleman told PsyPost. “This is valuable because it provides useful genetic information that others can use to study anorexia nervosa more deeply. However, we also wanted to extend beyond anorexia nervosa and also beyond diagnoses (which are based on grouping observed symptoms rather than being based in biology).”
“For that reason, we wanted to carry out a large genetic study of binge eating, as this is a key, under-studied symptom that is present across different eating disorders (anorexia nervosa, bulimia nervosa, binge-eating disorder) in different contexts (notably, the relationship with BMI is different across these disorders),” he added. “Having a large genetic study of binge eating would allow us to understand how the genetics of an eating behavior (binge eating) related to those of an eating disorder (anorexia nervosa), as well as how a common eating symptom (binge eating) related to other common symptoms and conditions such as body composition measures.”
The researchers conducted a genome-wide association meta-analysis, which pools results from many studies that each scanned the genomes of many people for genetic variations associated with a trait. They analyzed 27 studies, 14 of which had been part of the consortium’s 2019 analysis, comparing the DNA of people who had a history of binge-eating behavior or anorexia to the DNA of people without these conditions.
The sample sizes were vast, with the binge-eating analysis including 39,279 cases and 1,227,436 controls, and the anorexia nervosa analysis including 24,223 cases and 1,243,971 controls. All participants in the primary analyses were of European ancestry.
Binge eating was defined broadly: people counted as cases if they described eating unusually large amounts of food with a sense of lost control, answered yes to a single question about binge eating, or reported a diagnosis of bulimia or binge-eating disorder, even without confirmation from a health professional. Most cases were women, making up 96 percent of the binge-eating group and 94 percent of the anorexia group.
The researchers analyzed millions of genetic markers to see if certain variations appeared more often in people with these eating behaviors. They also calculated genetic correlations, comparing the genetic patterns of the eating disorders with those of other traits like psychiatric conditions and BMI. To see if the genetic risk for eating disorders was just a side effect of genes that control weight, they mathematically separated out the genetic influence of BMI.
The analysis identified six independent genetic regions associated with binge-eating behavior. Some had previously been tied to smoking, risk-taking, and the age at which girls have their first period. One lies near FTO, a gene region well known for its links to obesity; it was associated with binge eating but not with anorexia, and the authors suggest that FTO’s connection to higher BMI may run partly through binge eating.
For anorexia, the researchers identified eight genetic regions: six that had appeared in the 2019 study and two new ones. Because the new analysis reused much of the same data, the repeat findings are not fully independent confirmation, and two regions from the earlier study no longer reached the threshold for significance. The team also found one region specifically tied to the restricting subtype of anorexia, in which people limit food intake without regular binge eating or purging.
When comparing the conditions, binge eating and anorexia shared some genetic influences. They showed a genetic correlation of 0.46, a measure of the extent to which the same genetic variants influence two traits, on a scale where 0 means no shared genetic influence and 1 means complete overlap. Both conditions shared positive genetic correlations with psychiatric issues like major depressive disorder, anxiety, and schizophrenia.
The findings are broadly in line with research covered by PsyPost in 2023, which found that people with major depression reported more disordered eating behaviors than healthy volunteers. That study measured symptoms directly in patients, whereas the new study examined overlap at the level of genetic variants.
However, the two conditions also differed psychiatrically. Anorexia, but not binge eating, was genetically linked to obsessive-compulsive disorder. Binge eating had a stronger link to ADHD and, unlike anorexia, was genetically linked to smoking, problem drinking, and general risk tolerance.
Despite their shared psychiatric links, binge eating and anorexia displayed opposing genetic correlations with body measurements. The genetic markers for binge eating tended to align with a higher BMI and higher body fat percentage. In contrast, the genetic markers for anorexia were associated with a lower BMI and lower body fat percentage, though anorexia showed no genetic overlap with naturally being very thin, suggesting its genetics reflect more than just low body weight.
The researchers also found that these eating disorder traits are largely distinct from simple weight regulation. Using a statistical technique to separate out genetic influences shared with BMI, they found that this shared component accounted for only about 12 percent of the genetic signal for binge eating and 10 percent for anorexia, leaving the large majority independent of body weight genetics.
“Anorexia nervosa is not just a consequence of a genetic predisposition to low body weight, and similarly binge eating is not just a response to a genetic predisposition to high body weight,” Coleman explained. “Each has genetic links to the other, and to other psychiatric disorders and traits, but each has unique genetic features too.”
Finally, the team generated polygenic risk scores, which summarize a person’s overall genetic risk based on many small genetic variations. When the researchers applied anorexia risk scores built from the European data to two small studies from Japan and Korea, with about 150 anorexia cases combined, higher scores were linked to higher odds of anorexia, though they explained only about 1.3 percent of the variation in risk. This suggests that some genetic factors for anorexia are shared across ancestries.
“The effects of individual variants on psychiatric traits and disorders in general are very small, but there are a lot of them, and together their effects become similar in size to other risk factors like adverse life events,” Coleman noted. “That is also true for anorexia nervosa and for binge eating.”
“Speaking practically, those individual effects are not very important – most people with the risk version of any given variant won’t binge eat,” he said. “However, the combined set of variants (what we call a polygenic score) has a moderate effect, and we hope that further research can show that it can be useful in future alongside known non-genetic risk factors like family history and history of life events.”
As with all research, there are some caveats to consider. The primary limitation is the heavy reliance on participants of European ancestry. Applying these findings to other global populations requires caution, as differences in genetic background and environments could influence genetic risk.
Because the studies used different ways of identifying cases, and some comparison participants were never screened for eating disorders, the groups may be more mixed than in a clinic-based study. The mostly female sample also means the results may not apply equally to men.
Diagnostic crossover is another factor to keep in mind. People’s eating disorder symptoms can change over time, meaning someone with the restricting subtype of anorexia might develop binge-eating symptoms years later. Because the data relies on cross-sectional studies that take a snapshot in time, some people in one category might eventually migrate to another, though the authors note that diagnostic crossover more likely hides real genetic differences than creates false ones.
Although the combined scores carry real information about risk at the population level, the authors note they remain weak predictors for individuals: in the European data, anorexia scores accounted for about 2.3 percent of the variation in risk and binge-eating scores only about 0.3 percent. They still cannot tell whether a particular person will develop an eating disorder without looking at other risk factors. The authors hope to conduct even larger studies incorporating multiple eating disorder diagnoses and global ancestries to build a more complete biological map.
“It is also important that people understand that this is very much work in progress,” Coleman said. “We don’t fully understand the genetics of either anorexia nervosa or binge eating, and we are still a long way off being able to use genetics to help treat these conditions.”
“But our understanding is sufficient to say that, while genetics plays a role in these conditions, neither is genetically determined, and supportive treatment and supportive social environments can help both,” he concluded.
The study, “Genomic meta-analyses of binge-eating behavior and anorexia nervosa yield insights into the unique and shared biology of eating disorder phenotypes,” was authored by Jet D. Termorshuizen, Helena L. Davies, Sang-Hyuck Lee, Jessica K. Dennis, Christopher Hübel, Jessica S. Johnson, Yi Lu, Melissa A. Munn-Chernoff, Triinu Peters, Baiyu Qi, Katherine E. Schaumberg, Rebecca H. Signer, Karanvir Singh, Abigail R. ter Kuile, Laura M. Thornton, Jiayi Xu, Shuyang Yao, Zeynep Yilmaz, Ruyue Zhang, Johan Zvrskovec, Mohamed Abdulkadir, Ziada Ayorech, Elizabeth C. Corfield, Alexandra Havdahl, Kristi Krebs, Taralynn M. Mack, Maria Niarchou, Teemu Palviainen, Julia M. Sealock, Jessica H. Baker, Andrew W. Bergen, Andreas Birgegård, Vesna Boraska Perica, Katharina Bühren, Roland Burghardt, Matteo Cassina, Giovanni Castellini, Enrico Collantoni, James J. Crowley, Unna N. Danner, Franziska Degenhardt, Janiece E. DeSocio, Christian Dina, Monika Dmitrzak-Węglarz, Laramie E. Duncan, Karin M. Egberts, Lenka Foretova, Ina Giegling, Fragiskos Gonidakis, Scott D. Gordon, Jakob Grove, Sébastien Guillaume, Jerry D. Guintivano, Annette M. Hartmann, Konstantinos Hatzikotoulas, Stefan Herms, Hartmut Imgart, Susana Jiménez-Murcia, Antonio Julià, Gursharan Kalsi, Deborah Kaminská, Leila J. Karhunen, Hannah L. Kennedy, Kirsty M. Kiezebrink, Theresa Kolb, Janne T. Larsen, Dong Li, Lisa Lilenfeld, Mario Maj, Morten Mattingsdal, Paolo Meneguzzo, Allison L. Miller, Karen S. Mitchell, Alessio Maria Monteleone, Catherine M. Olsen, Leonid Padyukov, Richard Parker, Michaela A. Pettie, Dalila Pinto, Anu Raevuori, Samuli Ripatti, Marion E. Roberts, Paolo Santonastaso, Androula Savva, Ulrike H. Schmidt, Alexandra Schosser, Jochen Seitz, Lenka LS Slachtova, Agnieszka Slopien, Sandro Sorbi, Peter S. Straub, Jin P. Szatkiewicz, Friederike I. Tam, Elena Tenconi, Alfonso Tortorella, Artemis Tsitsika, Annemarie A. van Elburg, Gudrun Wagner, Hunna J. Watson, Roger AH Adan, Lars Alfredsson, Ole A. Andreassen, Helga Ask, Anders D. Børglum, Harry A. Brandt, David Collier, Steven Crawford, Scott Crow, Lea K. Davis, Martina de Zwaan, George Dedoussis, Danielle M. Dick, Stefan Ehrlich, Xavier Estivill, Angela Favaro, Fernando Fernández-Aranda, Krista Fischer, Andreas J. Forstner, Philip Gorwood, Hakon Hakonarson, Johannes Hebebrand, Beate Herpertz-Dahlmann, Anke Hinney, James I. Hudson, Craig Johnson, Jennifer Jordan, Allan S. Kaplan, Jaakko Kaprio, Andreas FK Karwautz, Martien JH Kas, Walter H. Kaye, James L. Kennedy, Martin A. Kennedy, Anna Keski-Rahkonen, Youl-Ri Kim, Kelly L. Klump, Mikael Landén, Stéphanie Le Hellard, Kelli Lehto, Qingqin S. Li, Jolanta Lissowska, Jurjen J. Luykx, Sarah L. Maguire, Nicholas G. Martin, Manuel Mattheisen, Sarah E. Medland, Philip Mehler, Nadia Micali, James E. Mitchell, Palmiero Monteleone, Preben Bo Mortensen, Benedetta Nacmias, Roel A. Ophoff, Hana Papezova, Nancy L. Pedersen, Liselotte V. Petersen, Luisa S. Rajcsanyi, Nicolas Ramoz, Ted Reichborn-Kjennerud, Valdo Ricca, Stephan Ripke, Dan Rujescu, Filip Rybakowski, Stephen W. Scherer, Margarita CT Slof-Op ‘t Landt, Howard Steiger, Patrick F. Sullivan, Beata Świątkowska, Eric F. van Furth, Tracey D. Wade, Thomas Werge, David C. Whiteman, D. Blake Woodside, Ya-Ke Wu, Stephan Zipfel, Cynthia M. Bulik, Laura M. Huckins, Gerome Breen, and Jonathan R.I. Coleman.
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Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BingeEatingGenes #GeneticLinksEatingDisorders #FTOgeneticRegion #AnorexiaNervosa #BingeEatingDisorder #BMIgenetics #PsychiatricGenomics #EatingDisorderResearch #GenomicMetaAnalyses #WeightAndBehavior genetics
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DATE: October 16, 2026 at 08:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: New compounds target clumping enzyme to protect brain cells in Alzheimer’s models
Researchers have identified a specific enzyme that clumps up and damages cellular powerhouses in the brains of mice with Alzheimer’s disease. Developing chemical compounds to prevent or eliminate these clumps slowed memory loss and brain cell death in the animals. The findings were published in Cell Reports Medicine.
Alzheimer’s disease involves the buildup of misfolded proteins in the brain, most notably beta-amyloid plaques and tau tangles. These proteins interfere with brain cell function and eventually lead to memory loss and cognitive decline.
A lesser-known player in cell survival is an enzyme called G-protein-coupled receptor kinase 2, or GRK2. In healthy cells, this enzyme usually operates in the main fluid of the cell, where it helps regulate cellular communication and stress responses.
When modified by a specific chemical tag in a process called phosphorylation, GRK2 changes its behavior. It can migrate to mitochondria, the microscopic structures that generate energy for cells.
A research team led by Joshua Abd Alla and Ursula Quitterer at ETH Zurich in Switzerland investigated whether abnormal regulation of this enzyme contributes to the brain damage seen in Alzheimer’s disease. Mitochondrial dysfunction is a major feature of the condition, and the researchers suspected that modified GRK2 might be interfering with these cellular powerhouses.
The team first examined the brain tissue of genetically modified mice that develop Alzheimer’s-like symptoms. They looked specifically at older mice that already exhibited heavy beta-amyloid buildup.
They found that a massive portion of the GRK2 in these mice had clumped together into large, dysfunctional aggregates. These clumps were highly concentrated on the mitochondria within the brain cells of the animals.
When the researchers looked at brain tissue samples from a small study of four human patients with dementia likely caused by Alzheimer’s, they observed the exact same pattern of clumped GRK2. In both the mice and the human samples, the accumulation of this enzyme was accompanied by mitochondrial dysfunction and elevated oxidative stress.
The researchers noted that the presence of beta-amyloid and toxic tau proteins actually triggered the initial phosphorylation and clumping of GRK2 in laboratory models. This suggests a destructive cycle where Alzheimer’s hallmark proteins damage mitochondria by causing GRK2 to clump, which in turn accelerates the buildup of more Alzheimer’s proteins.
To understand how the clumped enzyme causes damage, the researchers analyzed which other proteins it bound to in the mouse brains. They discovered that it attached to a protein called TOMM6, which normally helps transport materials across the outer membrane of mitochondria.
The researchers then tested the chemical interaction between GRK2 and TOMM6 in laboratory dishes. They observed that active, healthy GRK2 typically adds a chemical tag to TOMM6, keeping it stable and functional.
The clumped, modified version of GRK2 found in the diseased brains was inactive and failed to modify TOMM6. Without this chemical tag, TOMM6 also began to clump up and lose its ability to interact with the mitochondrial pores.
The scientists next bred new strains of mice to genetically force different versions of the GRK2 enzyme into their brains. When they introduced an inactive, clumping version of GRK2, the mice developed severe mitochondrial damage, rapid beta-amyloid accumulation, and died at an accelerated rate.
Conversely, breeding mice to produce extra active, healthy GRK2 protected the animals against these symptoms and improved their survival. In another genetic test, the researchers engineered mice to produce extra TOMM6 to compensate for the amount lost to clumping.
While extra TOMM6 reduced the large plaques of beta-amyloid, it unexpectedly caused a different, soluble form of beta-amyloid to build up. This soluble buildup was highly toxic to the brain cells, leading to an increased mortality rate in the animals.
Because simply adding TOMM6 was harmful, the team tried a pharmacological approach to fix the root of the problem. They developed a small chemical compound called CPD10, designed to stabilize GRK2 and prevent it from adopting the harmful, clumping shape.
Using computer modeling, the researchers found that CPD10 preferentially attaches to the healthy, unphosphorylated form of GRK2. By binding to this active form, the compound shifts the cellular balance, making it much harder for the enzyme to become phosphorylated and clump together.
They administered this compound to aging Alzheimer’s mice over a six-month period. The compound successfully penetrated the brain and prevented the enzyme from clumping on the mitochondria.
The mice treated with CPD10 had healthier mitochondria, fewer beta-amyloid plaques, less toxic tau protein, and experienced less brain cell loss than untreated mice. Behavioral tests in a water maze showed that the treated mice also retained better spatial memory.
The researchers explored a second chemical strategy aimed at removing the existing clumps rather than preventing new ones. They synthesized another molecule, CPD57, designed to boost the activity of the proteasome, which acts as the garbage disposal system of the cell.
Cells naturally use the proteasome to break down damaged or unnecessary proteins, preventing toxic buildups. The CPD57 compound physically binds to the opening of this disposal system, acting like a gate opener to let more waste inside.
They treated older Alzheimer’s mice with this compound for 14 days and evaluated their brain tissue. The compound increased the cellular garbage disposal activity and successfully degraded the clumped GRK2 and TOMM6 proteins.
When given over a six-month period, this molecule also slowed the accumulation of beta-amyloid plaques and reduced signs of cellular aging. The findings demonstrate that targeting these protein clumps from multiple pharmacological angles can offer neurological protection in animal models.
While these chemical compounds showed promising results in mice, animal models of Alzheimer’s disease do not perfectly replicate the human condition. The human tissue analysis in this study relied on a very limited number of brain samples obtained during surgery for brain tumors.
Because these samples were taken during active operations rather than after death, they provided a rare snapshot of the living brain’s chemistry, but the sample size was inherently small. Larger studies involving more human patients are necessary to confirm how widespread this specific enzyme clumping is in the general population.
It remains an open question whether the clumped enzyme on the mitochondria is the primary driver of the brain damage, or if the overall lack of healthy, active GRK2 floating elsewhere in the cell is the real culprit. Future research using organisms entirely deficient in GRK2 will help pinpoint the exact mechanism behind the cellular deterioration.
Extensive safety and efficacy testing will be required before either of the newly developed chemical compounds can be considered for human clinical trials. These findings provide a new pharmacological avenue to protect the aging brain.
The study, “Analysis of GRK2 aggregation in the pathology of Alzheimer disease in animal models,” was authored by Joshua Abd Alla, Alexander Perhal, Xuebin Fu, Andreas Langer, Yasser el Faramawy, and Ursula Quitterer.
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Worked great! Nice job by the micro.blog folks on making cross posting super easy!
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I’m back on Mastodon - Doing a quick check of the micro.blog cross post. Then it’s probably time for breakfast and back to work! https://hachyderm.io/@amatern