Multiple System Atrophy
Multiple System Atrophy - Related Videos
01:21
Detection of Brain Atrophy by Hematoxylin and Eosin Staining
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2025
To detect brain atrophy, begin with slides carrying the deparaffinized brain sections from neurodegenerative mouse models at various ages.
10:50
Tibial Nerve Transection - A Standardized Model for Denervation-induced Skeletal Muscle Atrophy in Mice
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Cited by 38 •
2013
The tibial nerve transection model is a well-tolerated, validated, and reproducible model of skeletal muscle atrophy. The model surgical protocol is described and demonstrated in C57Black6 mice.
01:23
Cellular Adaptation I: Introduction and Atrophy
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2026
Cells can adapt to environmental changes to maintain function and avoid injury, a process called cellular adaptation. Adapted cells exist in a reversible intermediate state with changes in size, number, phenotype, metabolism, or function. These responses help cells meet altered physiological or pathological demands; for example, enlargement of breast and uterine tissues during pregnancy. Early adaptations may enhance function, but persistent stress eventually causes tissue damage.Types of...
02:44
Injecting Recombinant Adeno-Associated Vectors in a Spinal and Bulbar Muscular Atrophy Mouse Model
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2025
Source:Pourshafie, N., et al. Systemic Delivery of MicroRNA Using Recombinant Adeno-associated Virus Serotype 9 to Treat Neuromuscular Diseases in Rodents. J. Vis. Exp. (2018).In this video, a spinal and bulbar muscular atrophy or SBMA-affected mouse undergoes tail vein injection of recombinant AAV (Adeno-associated vectors) vectors carrying a plasmid encoding therapeutic microRNA. The vector produces microRNA that binds to mutant AR (Androgen receptor)-mRNA (messenger ribonucleic acid),...
11:35
The Multiple Sclerosis Performance Test (MSPT): An iPad-Based Disability Assessment Tool
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Cited by 106 •
2014
Precise measurement of neurological and neuropsychological impairment and disability in multiple sclerosis is challenging. We report methodologic details on a new test, the Multiple Sclerosis Performance Test (MSPT). This new approach to the objective of quantification of MS related disability provides a computer-based platform for precise, valid measurement of MS severity.
FAQs
Its location links the disease to a specific cellular context rather than describing protein accumulation alone. Oligodendrocytes are therefore central to investigating how abnormal alpha-synuclein relates to degeneration of motor and autonomic neural circuits. This focus can help explain why movement, coordination, and blood-pressure regulation become affected together.
MSA research examines degeneration across circuits that regulate movement, coordination, and autonomic activity. Damage affecting these systems can produce overlapping clinical features, including parkinsonism, cerebellar ataxia, and orthostatic hypotension. Considering the pattern as a circuit-level problem helps neuroscience connect cellular pathology with the varied functions disrupted during disease progression.
Because MSA is studied alongside Parkinson’s disease and related disorders, researchers examine its broader clinical pattern rather than relying on parkinsonism alone. The presence of cerebellar ataxia and autonomic dysfunction provides additional context for investigation. Biomarker development may further improve the distinction between these neurodegenerative conditions.
Biomarker studies aim to improve the ability to identify MSA and distinguish it from Parkinson’s disease and related disorders. They may also provide clues about underlying disease mechanisms, including the relationship between alpha-synuclein accumulation and neural degeneration. Better biomarkers could support more precise research classification and evaluation of prospective treatments.
Researchers pay attention to the combination of parkinsonism, cerebellar ataxia, and autonomic dysfunction, particularly orthostatic hypotension. This combination captures the disease’s effects across movement, coordination, and blood-pressure regulation rather than focusing on a single manifestation. In clinical neuroscience, that broader pattern supports comparison among MSA and related neurodegenerative disorders.
MSA is currently incurable, so research must address both understanding and intervention. Investigators seek to clarify how abnormal alpha-synuclein and neural-circuit degeneration produce clinical symptoms, while also improving diagnostic biomarkers and developing treatments. These goals connect basic neuroscience with clinical neurology and may advance future approaches to disease assessment and treatment.