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Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

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Amyloid Fibrils03:03

Amyloid Fibrils

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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
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Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
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Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

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The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
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Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

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Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
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Proteoglycans01:05

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Glycans, a class of complex heterogeneous molecules, can be covalently attached to proteins to form glycosylated proteins that regulate various physiological and pathological processes. Glycosylated proteins or glycoproteins comprise N-linked and O-linked oligosaccharides. O-glycosylation is the most common type of protein glycosylation. Here, glycans attach to the oxygen atom of the hydroxyl groups of Serine or Threonine residues. O-linked glycosylation occurs later in protein processing,...
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Rapid Generation of Amyloid from Native Proteins In vitro
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[Amyloidoses].

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    Amyloidoses involve protein aggregate buildup. Advances in treating immunoglobulin light-chain amyloidosis (AL) and hereditary forms offer new hope for patients.

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    Area of Science:

    • Rare diseases characterized by extracellular protein aggregate deposition.
    • Fibrillary organization and beta-pleated sheet conformation define amyloid.
    • Focus on immunoglobulin light-chain amyloidosis (AL) and transthyretin amyloidosis.

    Context:

    • AL amyloidosis treatment improved with serum light chain assays and novel anti-plasma cell drugs.
    • Cardiac damage markers like BNP, NT-proBNP, and troponin aid prognostic assessment.
    • AA amyloidosis screening involves checking for proteinuria in chronic inflammatory disease patients.

    Purpose:

    • To summarize current understanding and advancements in diagnosing and treating various amyloidosis types.
    • Highlighting the importance of molecular typing and diagnostic tools.
    • Discussing recent therapeutic progress in managing amyloidosis.

    Summary:

    • Amyloidosis classification is based on protein aggregate type, with AL amyloidosis being most common.
    • Improved monitoring and new drugs enhance AL amyloidosis treatment.
    • Screening for AA amyloidosis and diagnosing hereditary forms require specific approaches.
    • Transthyretin stabilizers show promise for hereditary amyloid neuropathy.

    Impact:

    • Enhanced treatment monitoring and new therapies are improving outcomes for AL amyloidosis.
    • Early detection strategies for AA amyloidosis are crucial.
    • Genetic and clinical data integration is key for diagnosing rare hereditary amyloidoses.
    • Targeted therapies offer new hope for specific amyloidosis subtypes.