#proteopathy

[292-ludovica]

are there like. neuropathologists/epidemiologists specialising in proteopathies on here

I crave Information

[biotech-news-feed]

Microglia and astrocytes tend towards greater reactivity in the aging brain, entering a more inflammatory state. This sustained inflammation is maladaptive and contributes to the development of neurodegenerative conditions. In the research noted her #BioTech #science

[pathologising]

proteopathy more like hoeteopathy tf u aggregating for.....slut activity fr....u collectivising? alright man.

[siphonophore-consciousness]

Welcome to The Butterfly System

Queer, plural, 90+ members, 3 sidesystems: Aeonian, Butterfly, Khaos

Interests: Proteopathies (prions especially), dysbarism, crowd crush, fungi, colonial organisms, bismuth, mercury, radiation

Media interests: Marvel (Venom, Scarlet Witch), Supernatural, Undertale/Deltarune, The Magnus Archives, FNAF, The Locked Tomb, Diminish, Mystery Flesh Pit National Park, Pokemon (VG and TCG)

Our blogs:

Our other sidesystem Khaos: @khaos-system

Fiction hyperfixations/other interests: @day-dreeming

Clara’s blog: @your-ghost-companion

Other’s/Willow’s/purple’s: @demiproductive

Troublemaker’s: @moth-bitch

Hope’s: @ahopelessforest

Fictive’s/green’s: @fae-circle

Venting, trauma, and mental illness blog: @fromthedepthsofhel

[azuritefoxgirl]

via Fight Aging!

[serinakemp]

How α-Synuclein Aggregration Kills Neurons in Parkinson's Disease

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Parkinson's disease is strongly linked to quality control of mitochondria in neurons. The condition is characterized by the loss of a vital population neurons responsible for generating the neurotransmitter dopamine, and it is this loss that produces the tremors and other motor dysfunction observed in patients. Parkinson's disease is also a proteopathy, however, in which α-synuclein clumps together to form solid deposits that harm brain cells. In the research noted here, scientists show that this α-synuclein aggregation kills neurons by damaging mitochondria and triggering mitochondrial mechanisms that produce the form of cell death called apoptosis. This might suggest a link to what is already known of the important portions of the biochemistry of Parkinson's disease; more active mitochondrial quality control might slow the harm done by α-synuclein by removing damaged mitochondria before they can trigger apoptosis.

Parkinson's disease isn't the only synucleinopathy in which α-synuclein aggregation harms the function of the brain. Synucleinopathies are not the only class of proteopathy in the brain: amyloids and tau also form aggregates that are involved in the development of neurodegenerative conditions such as Alzheimer's disease. Finding ways to safely and reliably remove the excess molecular waste that accumulates within and between brain cells is a very important topic in medical research. Controlling one form of waste should provide benefits to patients suffering any of several varieties of neurodegeneration, but since aging brains tend to exhibit the signs of all of these forms of protein aggregate, clearing out all of them is most likely necessary in order to prevent or cure the most common age-related neurodegenerative conditions.

For years, scientists have known that Parkinson's disease is associated with a build-up of alpha-synuclein protein inside brain cells. But how these protein clumps cause neurons to die was a mystery. Using a combination of detailed cellular and molecular approaches to compare healthy and clumped forms of alpha-synuclein, researchers have discovered how the protein clumps are toxic to neurons. They found that clumps of alpha-synuclein moved to and damaged key proteins on the surface of mitochondria - the energy powerhouses of cells - making them less efficient at producing energy. It also triggered a channel on the surface of mitochondria to open, causing them to swell and burst, leaking out...

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[scaly-and-redhead]

New research has uncovered a quality control mechanism in brain cells that may help keep deadly neurological diseases in check for months or years.

[pathologising]

angle can u tell us about prion disease and protein misfolding the words sound cool but idk what they mean but im curious thank u bestie <33

proteins are in ur body RN doing so many things so many its crazy! Sometimes these proteins fuck up majorly for a variety of reasons and misfold. Diseases caused by this misfolding are called proteopathies (prion diseases are a form of proteopathy!). From this paper by T. Chaudhuri et al. "Protein misfolding is believed to be the primary cause of Alzheimer's disease, Parkinson's disease, Huntington's disease, Creutzfeldt-Jakob disease, cystic fibrosis, Gaucher's disease and many other degenerative and neurodegenerative disorders"

As u can see....not good lol. As for prion diseases, also known as transmissible spongeiform encephalopathies (TSEs), they're a special case (and the loves of my life By The Way.)!!! Pathogenic prions (prpsc) act in a way that can be described as infective (like a virus!!!!), coming into contact with other normal prion proteins (prpc) and turning them into prpsc (like a zombie...woah). BUT infective prions dont have genetic material that we know of (bc they're proteins lol)...which is crazy!!!!!!! They have no DNA .....no RNA...which is very unlike all other infectious agents (like bacteria viruses, or fungi!). so thats....fucking strange frankly what's up with that ! ALSO they literally are strong as all hell...resisting temperatures of up to 900°F! I do believe they're also protease-resistant and detergent-insoluble which means they're beefy (heh...) asf.

But yeah there's a few different prion diseases in both animals and humans (you might've heard of some! Mad Cow Disease (bovine spongeiform encephalopathy) in cows or Chronic Wastings Diseases (zombie deer disease woaah) in deer and some other animals !!!!). Basically you get them and they're invariably fatal, like... you will die, period. There's no cure but luckily prion diseases are pretty rare. This is super informal bc I'm on mobile but if you have specific questions lmk I will do my best to answer <3

[batscheisse]

MHS 20: BIOCRIMES, BINARY BIOLOGY, PROTEOPATHY, MORGELLONS, MONSANTO NARRATED

MHS 20: BIOCRIMES, BINARY BIOLOGY, PROTEOPATHY, MORGELLONS, MONSANTO NARRATED

Morgellons Info + Dokumente Intelligenter Staub – #Morgellon ist ein Pilz, der “höhere DNA assimilieren, multiplizieren und einen DNA-Cluster aufbauen kann, der im frühen Embryo eine Differenzierung von Zellen und Geweben bewirkt, die die Form und Struktur der verschiedenen Organe und Teile vom Körper festlegt . Der Pilz verwendet…

[azuritefoxgirl]

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[serinakemp]

Mapranosis: the Influence of Commensal Microbes on Neurodegenerative Disease

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Commensal microbes are the largely helpful populations that live inside us, usually meaning the gut microbiota, but there are others, such as the bacteria found in the mouth. Among these largely helpful microbes are a range of species that cause us harm over the years, however - consider the bacterial origins of gum disease, for example. Researchers are increasingly interested in the ways in which the swarming microbial life inside us, and particularly in the gut, might influence the progression of aging; to what degree are gut bacteria a cause of the observed natural variations in pace and outcome of aging in mammals? This is an open question.

In the case of neurodegenerative conditions such as Alzheimer's disease, microbial life may contribute by generating some fraction of the amyloid deposits or chronic inflammation known to be associated with the condition. In this context, some scientists are focused on invading microbes such as spirochetes, while others, like those noted here, are more interested in the commensal microbes that normally live inside us. There is a fair amount of evidence for either of these two classes of microbe to be involved.

Research in the past two decades has revealed that microbial organisms in the gut influence health and disease in many ways, particularly related to immune function, metabolism, and resistance to infection. Recent studies have shown that gut microbes also may cause or worsen Parkinson's disease, Alzheimer's disease and other neurodegenerative conditions. Researchers now propose the term "mapranosis" for the process by which amyloid proteins produced by microbes (bacteria, fungi and others) alter the structure of proteins (proteopathy) and enhance inflammation in the nervous system, thereby initiating or augmenting brain disease. The term is derived from Microbiota Associated Protepathy And Neuroinflammation + osis (a process).

Research into the multitude of microbes that inhabit the human body has expanded considerably in recent years. Genomic analysis has begun to reveal the full diversity of bacteria, viruses, fungi, archaea, and parasites living in and on the body, the majority of them in the gut. Even more recently, researchers have begun to explore how the proteins and other metabolites produced by microbes inhabiting the gut influence functions in other parts of the body, including the brain. However, we do not yet have a full understanding of how these systems work. The...

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