#Tau Protein

[medicomunicare]

Cholesterol in brain network: how does its presence affects health or neurodegeneration?

Cholesterol in brain health and disease Cholesterol is found in the cell membranes of all human cells. It plays an integral role in neuronal signaling and synaptic connections, especially in the brain. Notably, the brain contains between 20-25% of all the body’s cholesterol reserves, making it the organ with the highest cholesterol concentration in the human body. Interestingly, peripheral…

[emed123]

Recent Insights in Alzheimer Research |

Discover the latest insights into Alzheimers research, shedding light on advancements in diagnosis and treatment.

[vidpoker11]

Simple test could help predict risk of Alzheimer’s disease 20 years in advance - ANU

A simple, cheap and non-invasive blood test could help predict a person’s risk of developing Alzheimer’s disease up to 20 years before symptoms show.     Physicists from The Australian National University (ANU) have come up with a way to use nanotechnology, combined with artificial intelligence (AI), to analyze proteins in our blood and search for signs of early neurodegeneration, or tell-tale…

[didanawisgi]

Alzheimer's Disease Puzzle: Delving into Pathogenesis Hypotheses

https://www.aginganddisease.org/EN/10.14336/AD.2023.0608

[wisedreamlandlove]

Therapien für Alzheimer: Was erwartet uns?

Trotz vieler vielversprechender Fortschritte bei der Behandlung der Alzheimer-Krankheit kommen neue Therapien nur langsam in Gang.

Vergleich eines gesunden Gehirns und eines Gehirns mit fortgeschrittenen Alzheimer-Schäden

Die derzeitigen Alzheimer-Therapien verbessern vorübergehend die Symptome des Gedächtnisverlusts und der Probleme beim Denken und Schlussfolgern.

Diese Alzheimer-Behandlungen steigern die Leistung von Chemikalien im Gehirn, die Informationen von einer Gehirnzelle zur anderen übertragen. Dazu gehören Cholinesterasehemmer und das Medikament Memantin. Diese Behandlungen können jedoch den zugrunde liegenden Verfall und das Absterben von Gehirnzellen nicht aufhalten. Je mehr Zellen absterben, desto weiter schreitet die Alzheimer-Krankheit fort.

Die Experten sind vorsichtig, aber hoffnungsvoll, was die Entwicklung von Behandlungen angeht, die das Fortschreiten der Alzheimer-Krankheit aufhalten oder verzögern können. Die Wissenschaft versteht immer besser, wie die Krankheit das Gehirn verändert. Dies hat zur Erforschung potenzieller Alzheimer-Behandlungen geführt, die den Krankheitsprozess beeinflussen können.

Künftige Alzheimer-Behandlungen könnten eine Kombination von Medikamenten umfassen. Dies ist vergleichbar mit der Behandlung vieler Krebsarten oder von HIV/AIDS, bei denen mehr als ein Medikament eingesetzt wird.

Die derzeitigen Alzheimer-Therapien verbessern vorübergehend die Symptome des Gedächtnisverlusts und der Probleme beim Denken und Schlussfolgern.

Diese Alzheimer-Behandlungen steigern die Leistung von Chemikalien im Gehirn, die Informationen von einer Gehirnzelle zur anderen übertragen. Dazu gehören Cholinesterasehemmer und das Medikament Memantin (Namenda). Diese Behandlungen können jedoch den zugrunde liegenden Verfall und das Absterben von Gehirnzellen nicht aufhalten. Je mehr Zellen absterben, desto weiter schreitet die Alzheimer-Krankheit fort.

Die Experten sind vorsichtig, aber hoffnungsvoll, was die Entwicklung von Behandlungen angeht, die das Fortschreiten der Alzheimer-Krankheit aufhalten oder verzögern können. Die Experten verstehen immer besser, wie die Krankheit das Gehirn verändert. Dies hat zur Erforschung potenzieller Alzheimer-Behandlungen geführt, die den Krankheitsprozess beeinflussen können.

Künftige Alzheimer-Behandlungen könnten eine Kombination von Medikamenten umfassen. Dies ist vergleichbar mit der Behandlung vieler Krebsarten oder von HIV/AIDS, bei denen mehr als ein Medikament eingesetzt wird.

Hier einige der Strategien, die derzeit untersucht werden.

Die Plaques ins Visier nehmen

Einige der neuen Alzheimer-Behandlungen zielen auf Verklumpungen des Proteins Beta-Amyloid, die so genannten Plaques, im Gehirn ab. Plaques sind ein charakteristisches Anzeichen der Alzheimer-Krankheit.

Amyloid-Plaques im Hirngebwebe

Zu den Strategien, die auf Beta-Amyloid abzielen, gehören:

Aktivierung des Immunsystems

Als monoklonale Antikörper bekannte Medikamente können verhindern, dass Beta-Amyloid zu Plaques verklumpt. Sie können auch bereits gebildete Beta-Amyloid-Plaques entfernen. Dazu helfen sie dem Körper, sie aus dem Gehirn zu entfernen. Diese Medikamente ahmen die Antikörper nach, die Ihr Körper natürlicherweise als Teil der Reaktion Ihres Immunsystems auf fremde Eindringlinge oder Impfstoffe produziert.

Im Juni 2021 hat die US-amerikanische Food and Drug Association (FDA) den monoklonalen Antikörper Aducanumab (Aduhelm) für die Behandlung der Alzheimer-Krankheit bei einigen Menschen zugelassen. Das Arzneimittel wurde bei Menschen mit früher Alzheimer-Krankheit, einschließlich Menschen mit leichter kognitiver Beeinträchtigung aufgrund der Alzheimer-Krankheit, untersucht.

Das Medikament wurde in den Vereinigten Staaten zugelassen, weil es die Beta-Amyloid-Plaques entfernt. Aber es wird nicht häufig eingesetzt. Die Studien über seine Wirksamkeit bei der Verlangsamung des kognitiven Verfalls sind uneinheitlich. Auch der Versicherungsschutz ist begrenzt.

Ein weiteres Alzheimer-Medikament, Lecanemab (Leqembi), hat sich als vielversprechend für Menschen mit leichter Alzheimer-Krankheit und leichter kognitiver Beeinträchtigung aufgrund der Alzheimer-Krankheit erwiesen. Die FDA hat das Medikament im Jahr 2023 zugelassen. Das Medikament wird über eine Infusion in den Arm verabreicht.

Eine klinische Studie der Phase 3 ergab, dass Lecanemab den kognitiven Abbau bei Menschen mit früher Alzheimer-Krankheit um 27 % verlangsamt. Das Medikament wirkt, indem es Beta-Amyloid-Plaques im Gehirn entfernt. Diese Studie war die bisher größte, in der untersucht wurde, ob die Entfernung von Beta-Amyloid-Plaques aus dem Gehirn den Krankheitsverlauf verlangsamen kann.

In einer weiteren laufenden Studie wird untersucht, wie wirksam Lecanemab bei Menschen mit einem Alzheimer-Risiko sein kann. Dazu gehören Menschen, die einen Verwandten ersten Grades, z. B. einen Elternteil oder ein Geschwisterkind, mit der Krankheit haben.

Donanemab, ein weiterer monoklonaler Antikörper, hat sich ebenfalls als vielversprechend erwiesen. Das Medikament wurde in eine Phase-3-Studie aufgenommen. Ergebnisse werden im Jahr 2023 erwartet.

Der monoklonale Antikörper Solanezumab zeigte jedoch keine Vorteile für Personen mit präklinischer, leichter oder mittelschwerer Alzheimer-Krankheit. Solanezumab senkte das Beta-Amyloid im Gehirn nicht, was der Grund dafür sein könnte, dass es nicht wirksam war.

Synapsen schützen

Ein ursprünglich als mögliches Krebsmittel entwickeltes Medikament - Saracatinib - wird nun bei der Alzheimer-Krankheit getestet.

Bei Mäusen schaltete Saracatinib ein bestimmtes Protein aus, wodurch die Synapsen wieder zu funktionieren begannen. Synapsen sind die winzigen Zwischenräume zwischen Gehirnzellen, über die die Zellen miteinander kommunizieren. Bei den Tieren in der Studie konnte ein gewisser Gedächtnisverlust rückgängig gemacht werden. Derzeit laufen Versuche mit Saracatinib als möglicher Alzheimer-Behandlung am Menschen.

Beta-Amyloid-Produktion verringern

Diese Therapien können die Menge des im Gehirn gebildeten Beta-Amyloids verringern. Die Forschung hat gezeigt, dass Beta-Amyloid in zwei Schritten, die von verschiedenen Enzymen ausgeführt werden, aus einem "Mutterprotein" gebildet wird.

Mehrere experimentelle Arzneimittel zielen darauf ab, die Aktivität dieser Enzyme zu blockieren. Sie sind als Beta- und Gamma-Sekretase-Inhibitoren bekannt. Jüngste Studien haben gezeigt, dass die Beta-Sekretase-Hemmer den kognitiven Verfall nicht verlangsamen. Außerdem waren sie mit erheblichen Nebenwirkungen bei Menschen mit leichter oder mittelschwerer Alzheimer-Krankheit verbunden. Dies hat den Enthusiasmus für diese Medikamente verringert.

Verklumpungen des Tau-Proteins verhindern

Ein lebenswichtiges Transportsystem der Gehirnzellen bricht zusammen, wenn sich ein Protein namens Tau in winzige Fasern verdreht. Diese Fasern werden Tangles genannt. Sie sind eine weitere häufige Veränderung in den Gehirnen von Menschen mit Alzheimer. Forscher suchen nach einer Möglichkeit, die Bildung von Tangles durch Tau zu verhindern.

Tau-Aggregationshemmer und Tau-Impfstoffe werden derzeit in klinischen Studien untersucht.

Entzündungen hemmen

Die Alzheimer-Krankheit verursacht eine chronische, schwache Entzündung der Gehirnzellen. Die Forscher untersuchen Möglichkeiten zur Behandlung der Prozesse, die bei der Alzheimer-Krankheit zu Entzündungen führen. Das Medikament Sargramostim (Leukine) befindet sich derzeit in der Forschung. Das Medikament könnte das Immunsystem dazu anregen, das Gehirn vor schädlichen Proteinen zu schützen.

Erforschung der Insulinresistenz

In Studien wird untersucht, wie Insulin das Gehirn und die Funktion der Gehirnzellen beeinflussen kann. Forscher untersuchen, wie Insulinveränderungen im Gehirn mit der Alzheimer-Krankheit zusammenhängen könnten. Bei einem Versuch mit einem Insulin-Nasenspray wurde jedoch festgestellt, dass das Medikament das Fortschreiten der Alzheimer-Krankheit nicht verlangsamen kann.

Erforschung der Verbindung zwischen Herz und Kopf

Es gibt immer mehr Hinweise darauf, dass die Gesundheit des Gehirns eng mit der Gesundheit von Herz und Blutgefäßen zusammenhängt. Das Risiko, an Demenz zu erkranken, scheint sich bei vielen Erkrankungen, die das Herz oder die Arterien schädigen, zu erhöhen. Dazu gehören Bluthochdruck, Herzerkrankungen, Schlaganfall, Diabetes und ein hoher Cholesterinspiegel.

In einer Reihe von Studien wird untersucht, wie man diesen Zusammenhang am besten ausbauen kann. Zu den untersuchten Strategien gehören:

Gängige Medikamente gegen Risikofaktoren für Herzkrankheiten. Forscher untersuchen, ob Blutdruckmedikamente Menschen mit Alzheimer helfen können. Sie untersuchen auch, ob die Medikamente das Demenzrisiko verringern können.

Medikamente für neue Ziele. In anderen Studien wird genauer untersucht, wie der Zusammenhang zwischen Herzerkrankungen und Alzheimer auf molekularer Ebene funktioniert. Ziel ist es, neue potenzielle Arzneimittel für Alzheimer zu finden.

Änderung des Lebensstils. Forschungsergebnisse deuten darauf hin, dass Lebensstilmaßnahmen, die bekanntermaßen für das Herz vorteilhaft sind, dazu beitragen können, der Alzheimer-Krankheit vorzubeugen oder ihren Ausbruch zu verzögern. Zu diesen Lebensstilentscheidungen gehören Sport und eine herzgesunde Ernährung.

Hormone

In den 1990er Jahren deuteten Studien darauf hin, dass die Einnahme einer Hormonersatztherapie während der Perimenopause und der Menopause das Risiko einer Alzheimer-Erkrankung senkt. Die weitere Forschung ist jedoch uneinheitlich. In einigen Studien wurde kein kognitiver Nutzen einer Hormonersatztherapie festgestellt. Weitere Forschungen und ein besseres Verständnis der Beziehung zwischen Östrogen und kognitiven Funktionen sind erforderlich.

Beschleunigung der Forschung

Die Entwicklung neuer Medikamente ist ein langsamer Prozess. Das Tempo kann für Menschen mit Alzheimer und ihre Familien, die auf neue Behandlungsmöglichkeiten warten, frustrierend sein.

Um die Forschung zu beschleunigen, hat das Konsortium Critical Path for Alzheimer's Disease (CPAD) in den USA eine Partnerschaft gegründet, um Daten aus klinischen Alzheimer-Studien auszutauschen. Zu den CPAD-Partnern gehören Pharmaunternehmen, gemeinnützige Stiftungen und Regierungsberater. CPAD hieß früher Coalition Against Major Diseases (Koalition gegen schwere Krankheiten).

CPAD hat auch mit dem Clinical Data Interchange Standards Consortium zusammengearbeitet, um Datenstandards zu entwickeln. Die Forscher sind der Ansicht, dass Datenstandards und die gemeinsame Nutzung der Daten von Tausenden von Studienteilnehmern die Entwicklung wirksamerer Therapien beschleunigen werden.

[xtruss]

Stanford Reverses Cognitive Decline in Alzheimer’s With Brain Metabolism Drug

Neuroscientists at Stanford have Linked Alzheimer’s Disease to the Disruption of Brain Metabolism via the Kynurenine Pathway, which is Affected by Amyloid Plaque and Tau Proteins.

— By Stanford University | August 22, 2024

Stanford Researchers Have Found That Blocking the Kynurenine Pathway in the Brain Can Reverse the Metabolic Disruptions Caused By Alzheimer’s Disease, Improving Cognitive Functions in Mice. Credit: SciTechDaily.com

Alzheimer’s Disease and Brain Energy Metabolism

Their research has demonstrated that drugs blocking this pathway can restore cognitive function in Alzheimer’s mice by improving brain metabolism. This discovery not only bridges the gap between neuroscience and oncology but also provides a fast track to repurposing existing drugs for Alzheimer’s treatment.

Neuroscientists believe one of the key mechanisms by which Alzheimer’s disease impairs brain function is through the disruption of glucose metabolism, which is essential for energizing a healthy brain. Essentially, a decrease in metabolism deprives the brain of vital energy, thereby hindering cognitive functions and memory.

Against that backdrop, a team of neuroscientists at the Knight Initiative for Brain Resilience at Stanford’s Wu Tsai Neurosciences Institute have zeroed in on a critical regulator of brain metabolism known as the kynurenine pathway. They hypothesize that the kynurenine pathway is overactivated as a result of amyloid plaque and tau proteins that accumulate in the brains of patients with Alzheimer’s disease.

Restoring Cognitive Function in Lab Mice

Now, with support from research and training grants from the Knight Initiative, they have shown that by blocking the kynurenine pathway in lab mice with Alzheimer’s Disease, they can improve, or even restore, cognitive function by reinstating healthy brain metabolism.

“We were surprised that these metabolic improvements were so effective at not just preserving healthy synapses, but in actually rescuing behavior. The mice performed better in cognitive and memory tests when we gave them drugs that block the kynurenine pathway,” said senior author, Katrin Andreasson, a neurologist at the Stanford School of Medicine and member of the Wu Tsai Neurosciences Institute.

The study, which included collaborations with researchers at the Salk Institute for Biological Studies, Penn State University, and others, was published on August 22, 2024, in the journal Science.

Hungry Neurons

In the brain, kynurenine regulates production of the energy molecule lactate, which nourishes the brain’s neurons and helps maintain healthy synapses. Andreasson and her fellow researchers specifically looked at the enzyme indoleamine-2,3-dioxygenase 1 — or IDO1, for short — which generates kynurenine. Their hypothesis was that increases in IDO1 and kynurenine triggered by accumulation of amyloid and tau proteins would disrupt healthy brain metabolism and lead to cognitive decline.

“The kynurenine pathway is over activated in astrocytes, a critical cell type that metabolically supports neurons. When this happens, astrocytes cannot produce enough lactate as an energy source for neurons, and this disrupts healthy brain metabolism and harms synapses” Andreasson said. Blocking production of kynurenine by blocking IDO1 restores the ability of astrocytes to nourish neurons with lactate.

Potential Fast-Tracking of IDO1 Inhibitors

Best of all for Andreasson, and for Alzheimer’s patients, IDO1 is well known in oncology and there are already drugs in clinical trials to suppress IDO1 activity and production of kynurenine. That meant Andreasson could circumvent the time-intensive work of identifying new drugs and to begin testing in lab mice almost immediately.

In those tests, in which mice with Alzheimer’s Disease must navigate an obstacle course before and after drug intervention, Andreasson and team found that the drugs improved hippocampal glucose metabolism, corrected deficient astrocytic performance, and improved the mice’s spatial memory.

Promising Results Across Different Pathologies

“We also can’t overlook the fact that we saw this improvement in brain plasticity in mice with both amyloid and tau mice models. These are completely different pathologies, and the drugs appear to work for both,” Andreasson noted. “That was really exciting to us.”

Better yet, this intersection between neuroscience, oncology, and pharmacology could help speed drugs to market if proved effective in ongoing human clinical trials for cancer.

“We’re hopeful that IDO1 inhibitors developed for cancer could be repurposed for treatment of AD,” Andreasson stressed.

A Glimpse into the Future of Alzheimer’s Treatment

The next step is to test IDO1 inhibitors in human Alzheimer’s patients to see if they show similar improvements in cognition and memory. Prior clinical tests in cancer patients tested the effectiveness of IDO1 inhibitors on cancer but did not anticipate or measure improvements in cognition and memory. Andreasson is hoping to investigate IDO1 inhibitors in human trials for Alzheimer’s disease in the near future.

Reference: “Restoring hippocampal glucose metabolism rescues cognition across Alzheimer's disease pathologies” 22 August 2024, Science. DOI: 10.1126/science.abm6131

Stanford Wu Tsai Neurosciences Institute / Knight Initiative for Brain Resilience Authors:

Paras S. Minhas (co-lead), Amira Latif-Hernandez (co-lead), Aarooran S. Durairaj, Qian Wang, Siddhita D. Mhatre, Takeshi Uenaka, Joshua Crapser, Travis Conley, Hannah Ennerfelt, Yoo Jin Jung, Yeonglong Albert Ay, Matthew Matrongolo, Edward N. Wilson, Tao Yang, Marius Wernig, Frank M. Longo, and Katrin I. Andreasson (corresponding).

Other Contributing Institutions

The Salk Institute for Biological Studies (including co-lead author Jeffrey R. Jones), Keio University, Princeton University, Penn State University, UC San Francisco, and the Banner Sun Research Institute.

Wu Tsai Neurosciences Institute / Knight Initiative for Brain Resilience Support:

The research was supported by an Innovation Award and a Brain Resilience Scholar Award from the Knight Initiative for Brain Resilience at the Wu Tsai Neurosciences Institute. The study made use of Wu Tsai Neurosciences Institute Community Laboratories: the Stanford Behavioral and Functional Neuroscience Laboratory and the Stanford Neuroscience Microscopy Service, as well as the Stanford Mass Spectroscopy Core.

— Competing Interests: Andreasson is a Co-Founder, Board Member, and Consultant for Willow Neuroscience, Inc. Longo is a Founder of, Board Member of, and Consultant for and has Financial Interest in PharmatrophiX, a Company Focused on Small-Molecule Development for Treatment of Neurodegenerative Disorders.

[mindblowingscience]

One dose of a new treatment, delivered by nasal spray, clears away build-ups of the toxic tau protein associated with Alzheimer’s disease from inside brain cells, improving memory, according to new research. It paves the way for new treatments for the debilitating disease. A few years ago, abnormal clumps of tau proteins in the brain were found to be associated with Alzheimer’s disease. Since then, researchers have been working on a way of eradicating these toxic tangles, which have become a hallmark of the degenerative disease.

Continue Reading.

[afeelgoodblog]

Wanted to give a bit of good news that was told today (7/11): Mice with Alzheimer's responded positively to a nasal spray invention. Here's the title - "Nasal spray found to clear tau proteins from Alzheimer's mouse model brains"

Found the paper for this:

thank you for submitting. I'll add this to my newsletter

[bubble-leaves]

Ok so headcanons but hassian.

You got it!

Hassian . . .

- absolutely cannot stand you when he first meets you; you seem to be like every other invasive human that reemerged

- acts coldly toward you, but secretly starts respecting you once you start engaging in Majiri traditions and bringing him gifts

- eventually starts opening up to you after you somehow weasel your way into his daily life

- pretends he's always annoyed by you, but only because you both adapted a dynamic where you're constantly bubbly and he's less than enthused; he clearly loves your attention either way

- can't get his mind off you when he's romanced

- is hesitant to be romantic with you at first, considering his cruel break-up with Tamala in the past. But you gradually let him know that you are nothing like her as you two continue bonding

- wants to learn more about your interests as much as he wants to share his

- wants to learn more about your culture; he secretly takes notes of whatever you can remember about your land and people

- writes secretly in general; little recordings of funny things you say or adorable things you do, a journal to rant about you in, and yes, meaningful poetry about you

- is completely head over heels if you're a proven hunter

- secretly talks with Tau about how crazy you make him feel; Tau doesn't say much (lol)

- values traditional Majiri romance, but also is curious about how humans court someone they admire; he'll ask and try to replicate any of the rituals, if he can

- is characteristically blunt when you explain pieces of your culture; he'll openly express his distaste for certain differences, although he tries to remain respectful

- is obsessed with your touch. Like, severely.

- feels his heart rate spike dramatically if you touch so much as his arm

- isn't reclusive when it comes to reciprocating physical affection; he'll just want your permission, first

- always makes a point to compliment you; it helps him come out of his shell a little and, hey, you look so precious when you light up and thank him

- smiles and laughs at any joke you make, no matter how stupid it is

- LOVES making you laugh; he's not much of a funny guy, so if he just so happens to say something that makes you laugh, he deeply blushes at the sound and chuckles with you

- as the relationship progresses, he feels terribly alone if he doesn't sleep next to you

- appreciates how you treat Tau as your own and likes to hear you talk to him, even if it's in a ridiculous high-pitched voice

- can cook, but mostly prepares proteins, so you'll have to cook the side dishes

- loves when you read to him, especially if it's one of the romance novels he's read a million times; hearing the stories told in your voice makes his heart rush all over again

- sleeps the best when he's on his back, holding you close with one arm and Tau in the other

- will sometimes not let you get up if you're spooning in the early morning; he will sleepily yet playfully tell you that you're not going anywhere until the sun comes up

[reasonsforhope]

Researchers from Western and Brown University have made groundbreaking progress towards identifying the root cause and potential therapy for preeclampsia.

The pregnancy complication affects up to eight per cent of pregnancies globally and is the leading cause of maternal and fetal mortality due to premature delivery, complications with the placenta and lack of oxygen.

The research, led by Drs. Kun Ping Lu and Xiao Zhen Zhou at Western, and Drs. Surendra Sharma and Sukanta Jash at Brown, has identified a toxic protein, cis P-tau, in the blood and placenta of preeclampsia patients.

According to the study published in Nature Communications, cis P-tau is a central circulating driver of preeclampsia – a “troublemaker” that plays a major role in causing the deadly complication...

“The root cause of preeclampsia has (so far) remained unknown, and without a known cause there has been no cure. Preterm delivery is the only life-saving measure,” said Lu, professor of biochemistry and oncology at  Schulich School of Medicine & Dentistry...

“Our study identifies cis P-tau as a crucial culprit and biomarker for preeclampsia. It can be used for early diagnosis of the complication and is a crucial therapeutic target,” said Sharma...

Until now, cis P-tau was mainly associated with neurological disorders like Alzheimer’s disease, traumatic brain injuries (TBI) and stroke. This association was discovered by Lu and Zhou in 2015 as a result of their decades of research on the role of tau protein in cancer and Alzheimer’s.

An antibody developed by Zhou in 2012 to target only the toxic protein while leaving its healthy counterpart unscathed is currently undergoing clinical trials in human patients suffering from TBI and Alzheimer’s Disease. The antibody has shown promising results in animal models and human cell cultures in treating the brain conditions.

The researchers were curious whether the same antibody could work as a potential treatment for preeclampsia. Upon testing the antibody in mouse models they found astonishing results.

“In this study, we found the cis P-tau antibody efficiently depleted the toxic protein in the blood and placenta, and corrected all features associated with preeclampsia in mice. Clinical features of preeclampsia, like elevated blood pressure, excessive protein in urine and fetal growth restriction, among others, were eliminated and pregnancy was normal,” said Sharma.

Sharma and his team at Brown have been working on developing an assay for early detection of preeclampsia and therapies to treat the condition. He believes the findings of this study have brought them closer to their goal...

“The results have far-reaching implications. This could revolutionize how we understand and treat a range of conditions, from pregnancy-related issues to brain disorders,” said Lu.

-via India Education Diary, September 22, 2023

[hellopersimmonpie]

Sejak meyakinkan diri sendiri bahwa w tidak sedang dalam mode survival, gue belajar merawat diri dengan lebih baik. Makan dengan kalori yang tidak berlebihan. Tidak demonizing makanan. Berusaha tidur dengan baik, mandi dengan baik, rutin membersihkan kamar dan memikirkan prioritas hidup yang entah harusnya kemana.

Jujur gue bingung antara ambil S3 atau serius ngejar profesi jadi Game Designer. Tapi diri gue kalo lagi autopilot ya mode Game Designer. Even kalo ketemu orang di lift mulai beberapa kali disapa:

"Udah daftar PhD?"

Sama halnya dengan di rumah:

"Udah punya calon?"

Yang pada akhirnya ngebuat gue semakin paham bahwa yang pertama banget perlu kita pelajari dalam hidup adalah....

"Hiduplah untuk diri kamu sendiri dulu. Baru setelah itu pikirkan yang lain"

Menjalani hidup semacam ini ternyata bukan hidup yang egois. Karena andai kita mencintai seseorang dan pengen bertahan lama bareng dia, pertama banget kita butuh badan dan mental yang sehat 😅 Kalo mau PhD, perlu tau dulu apa yang mau kita cari. Meskipun ya nggak semuanya dapet Profesor yang beneran linear sama bidang risetnya.

Lupakan perkara PhD. Mungkin ini kelihatan cukup lebay karena gue sampe nyimpen beberapa jenis suplemen di laci meja. But it helps me a lot buat bertahan menjadi waras di tengah kesibukan.

Belakangan ini, gue tuh jaga makan banget. Ga makan gorengan sama sekali. Ga makan pedes. Double protein di piring dan selalu makan sayur. Gue juga mengurangi frekuensi ngopi maksimal 3 kali seminggu. Nggak kayak biasanya yang 2x sehari minum americano ato latte.

Gue minum vitamin B jadwal lagi padat-padatnya. Ternyata tidur gue lebih nyaman dan pencernaan gue lancar.

Gue juga beli produk buat ngerawat diri dan hiburan juga 😂 Sumpah gue happy banget kalo lagi capek terus mainin busanya Lovojoy. Lucu banget. Pink dan creamy. Thanks banget buat yang ngembangin produk Shower Mousse selucu ini

Meskipun gue berusaha biar badan dan otak gue bisa dipaksa kerja 12 jam tanpa stress, w masih berharap kelak jam kerja w berkurang, kebutuhan gue sama keluarga tercukupi dengan baik. Dan gue bisa masak makanan yang enak buat orang rumah.

Let's have a peaceful live, Dea!

[medicomunicare]

Biologicals to have a lag-3 timelapse from spreading: the new strategy to prevent Parkinson onset

In studies with genetically engineered mice, Johns Hopkins Medicine researchers say they have identified a potentially new biological target involving APLP1, a cell surface protein that drives the spread of Parkinson’s disease-causing alpha-synuclein. The findings reveal how APLP1 connects with Lag3, another cell surface receptor, in a key part of a process that helps spread harmful…

[covid-safer-hotties]

Does Long COVID Lead to Alzheimer’s? A New Study Took an Unexpected Turn - Published Aug 29, 2024

More than one in ten people who catch COVID don’t fully recover — developing a chronic condition called Long COVID which causes a variety of debilitating symptoms, including brain fog. Since some studies have found that COVID infections are associated with overall brain shrinkage, altered brain structure, and an increased risk of developing Alzheimer’s, researchers have been investigating the links between COVID and Alzheimer’s.

“There was a lot of discussion about whether COVID or even Long COVID would lead to a sudden onset form of Alzheimer’s disease so we set out to determine whether that was the case,” Dr. William Hu, director at the Center for Healthy Aging Research at Rutgers University told Being Patient.

Hu’s new study, published in Cell Reports Medicine, analyzed the cerebrospinal fluid and immune cells of Long COVID patients with brain fog. Rather than finding the telltale signs of Alzheimer’s, he discovered the patient’s immune system was still trying to fight off the COVID infection, which occurred about nine months prior. The patients whose immune cells mounted an antiviral response started to feel better — opening the door to new potential treatments for Long COVID that boost the body’s antiviral response.

What the study found The researchers looked at a group of participants from COVID recovery clinics, comparing 100 without any cognitive complaints, 79 who had abnormal results on a cognitive assessment indicating cognitive impairment, and 57 who complained about cognitive issues even though they scored normally on a cognitive test.

Hu and his colleagues took cerebrospinal fluid and blood from both groups of people with cognitive complaints to measure protein biomarkers and look at what genes the immune cells are turning on or off to see whether there was an overlap with Alzheimer’s disease. “We did not find significant numbers of people with Alzheimer’s disease markers in the cerebrospinal fluid,” Hu said. “The many molecular pathways being active in Long COVID do not correspond to Alzheimer’s disease.”

But nine months after the initial infection, what the researchers did notice was that the immune cells behaved as if they were still fighting off a viral infection. About 50 percent of the cognitively impaired participants showed slow improvement after two years. The participants whose immune cells mounted an interferon response — a pathway used by the immune system to fight viruses — showed cognitive improvement.

“One of the key findings is that we see the immune cells in the cerebrospinal fluid, recruiting cells to fight infection,” Hu said. “So that tells me that the infection is in the brain.”

One limitation of the study is that it may not capture the experience of people with more severe Long COVID impairments — since Long COVID leads to extreme fatigue, some might not be able to participate in these studies.

Long COVID and Alzheimer’s This study suggests that the mechanisms of Long COVID and Alzheimer’s disease are distinct. COVID-19 doesn’t seem to increase the levels of Alzheimer’s biomarkers.

“I think we can convincingly say right now that COVID does not cause acute Alzheimer’s disease,” Hu said. “Now whether it increases the risk for future Alzheimer’s disease is an open question.”

According to Hu, “there are many people walking around their 60s and 70s, with [asymptomatic] Alzheimer’s disease,” which means they have amyloid and tau in the brain but no symptoms. “A systemic illness [like COVID] can accelerate the manifestation of what previously was asymptomatic Alzheimer’s disease,” he said.

Although COVID-19 doesn’t directly cause Alzheimer’s disease, like other viral infections it may increase the risk of developing symptoms. This may explain why vaccines against the flu and other viral illnesses decrease the risk of developing Alzheimer’s disease.

Interferon and antiviral drugs for treating long COVID There are currently no treatments available for Long COVID. While the National Institutes of Health has poured more than $1 billion into testing new treatments, the program has been criticized by scientific experts and patients as many of these studies are testing treatments like “exercise��� and “cognitive behavioral therapy” which they say are ineffective and potentially harmful ((The National Institutes of Health’s Long COVID initiative RECOVER revised its exercise and exertion trials to reduce the risk of harm to participants.)

Hu said that patients should contact their elected representatives, senators, and congresspeople to ask them to accelerate new trials focused on developing antiviral therapies that might move the needle.

“Based on our data, it looks like a successful mounting of interferon-related pathways was associated with faster recovery,” he said. “Interferon itself can be tried and there are multiple forms of the drug.”

Interferon is already approved for treating multiple sclerosis, hepatitis C, non-Hodgkin’s lymphoma, and other autoimmune diseases. Interferon is also available in subcutaneous forms, which means that getting the drug wouldn’t require traveling to an infusion center for treatment.

How to prevent long COVID COVID-19 vaccines may prevent severe illness and death, but Hu said that so far large studies suggest that vaccines do not prevent Long COVID in particular.

“What prevents Long COVID is not catching COVID,” said Hu. Experts suggest using multiple layers of protection to reduce the chances of catching COVID-19. “Two things that have consistently worked is good air ventilation, and masking,” Hu said. “They’ve consistently shown to be effective in preventing infection.”

High-quality surgical masks and respirators effectively reduce the transmission of airborne diseases like COVID-19 and can also protect your lungs and brain during wildfire season. Ensuring proper air ventilation by opening windows, using HEPA filters, and improving airflow with fans makes it harder for infectious particles or pollutants to linger in the air.

Link to study: https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(24)00253-2

[in-tua-deep]

Huh in interesting scientific news there are differences between the tau proteins present in the brain caused by Alzheimer’s and ones caused by chronic traumatic encephalopathy (hella concussions)

and my father, the overachiever, had both! so now he gets to have a study on him published since he’s the first subject they’ve had with both!

he always did like to be first :’)

[warningsine]

A small new trial published in the journal Nature Medicine describes what would be two firsts for Parkinson's disease, if they pan out: a diagnostic test and a potential immune-based treatment that works similarly to a vaccine. The research is still early, but researchers are excited by the prospect of advances for a disease that lacks good diagnostics and treatments.

The target of both innovations is alpha synuclein, a protein that takes an abnormal form in Parkinson's patients—aggregating in their brains and destroying nerve cells involved in motor and some cognitive functions. While researchers have long known that these proteins are involved in the disease, finding ways to measure and target them has not been easy.

The (potential) Parkinson's vaccine

The Florida-based biotech company Vaxxinity developed a vaccine, or what it calls an active immune medicine, to train the immune system to attack only abnormal versions of the protein—which are improperly folded—and not the regular forms. This would essentially help people's bodies treat themselves.

“The idea is that patients should recognize their own misfolded proteins, and it is personalized because their own immune systems are doing the work,” says Dr. Mark Frasier, chief scientific officer at the Michael J. Fox Foundation for Parkinson’s Research, which funded the testing part of the study.

The Parkinson's test

The new diagnostic test for Parkinson’s, which was developed by researchers at University of Texas and Vaxxinity, uses samples of cerebrospinal fluid to measure a person's levels of abnormal alpha synuclein. If the U.S. Food and Drug Administration (FDA) grants it full approval, it will become the first test for diagnosing Parkinson's. (The FDA classified it as a breakthrough device in 2019, a status that expedites access to innovative technologies where there is unmet need.) “Without [such a test], you’re kind of shooting in the dark,” says Mei Mei Hu, CEO and co-founder of Vaxxinity.

Alpha synuclein has been tricky to measure in the body for several reasons, says Frasier. While everyone has the protein, abnormal forms of it occur in relatively small amounts, so they're harder to detect via imaging. This type of alpha synuclein also tends to clump inside cells rather than outside of them, making it even harder to see. If clumps are large enough to become detectable, they can look structurally similar to amyloid or tau—the proteins implicated in Alzheimer’s disease—so imaging tests might misdiagnose people with Alzheimer’s rather than Parkinson’s.

Read More: Michael J. Fox: Chasing Parkinson's Treatments

The test overcomes those hurdles by cleverly exploiting normal forms of the protein. Parkinson’s experts believe that tiny amounts of abnormal alpha synuclein circulate in the spinal fluid of patients, but are too small to be detected through imaging. To run the new test in the study, researchers take normal forms of the protein in the lab and add them to samples of spinal fluid from patients; that prompts any misfolded protein that might be present in the samples to pull the normal proteins into misfolded aggregates, amplifying the signal for the abnormal form. Scientists then use a fluorescent probe to detect how much antibody to the misfolded protein patients generated, resulting in a biomarker, or stand-in for the treatment effect.

This test would be a critical advance because it makes it possible to identify patients with abnormal alpha synuclein at the earliest stages of the disease, when treatments might be more effective.

With more data from patients, researchers hope to further refine what different levels mean, so that the test will be able to tell not just if a person has Parkinson's but whether someone might be at a greater risk of developing it. Currently the test is only used in research studies, but more results like these—as well as data on whether the same process can be applied to blood samples—could speed the test to getting approved for wider use.

What the study found

The trial—conducted by researchers at the University of Texas, the Mayo Clinic, the Michael J. Fox Foundation for Parkinson’s Research, and Vaxxinity—included 20 people with Parkinson’s. It was just designed to test the safety of the approach, so the study only provided hints about the treatment's effectiveness. Everyone received three shots over nearly a year; some contained the treatment at different doses, and some contained a placebo.

Overall, people receiving the vaccine generated more antibodies against the abnormal alpha synuclein protein than those vaccinated with placebo, as measured by the Parkinson's test. Antibodies started to ramp up about four months after the vaccinations began.

“What is unique about our technology is that it can stimulate the immune system to produce very, very specific antibodies against toxic forms of alpha synuclein, and do it in a safe way, which is reassuring,” says Jean-Cosme Dodart, senior vice president of research at Vaxxinity and senior author of the paper.

According to the test results, about half of the patients in the trial showed high levels of antibodies against the misfolded alpha synuclein, and most of these patients received the highest dose of the vaccine. They also scored the highest on motor and cognitive tests. There were too few patients to adequately assess any changes of Parkinson’s symptoms, but the researchers believe that longer follow-up with those tests, and potentially more frequent or higher doses of the vaccine, could lead to improvements in those scores. “The results are very, very encouraging,” says Dodart.

“This paper demonstrates that in a small number of people, the vaccine is having an impact on misfolded alpha synuclein, which is really exciting,” says Frasier. “We are now in the biological era for Parkinson’s disease."

[bpod-bpod]

Tracking Tau

Imaging and tissue section analysis of brains from patients who died with a diagnosis of Alzheimer's disease maps, across stages of the disease, the protein tangles called tau neurofibrils that have been shown to begin to accumulate first in the brain region called the medial temporal lobe

Read the published research article here

Image adapted from work by Sadhana Ravikumar and colleagues

Department of Radiology, University of Pennsylvania, Philadelphia, PA, USA

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in Nature Communications, June 2024

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