Results of Treatment of Certain Diseases of the Central Nervous System With Acth and Corticosteroids

Baumann, Jörg

doi:10.1111/j.1600-0404.1965.tb01914.x

Cited by 8 publications

(7 citation statements)

References 12 publications

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“…However, immunosuppressive drugs such as corticosteroids, azathioprine, cyclophosphamide, or combinations of them, as well as plasmapheresis therapy or intravenous immunoglobulins (IVIG), have failed to affect the progression of the disease [7–11]. Sequential treatment with plasmapheresis followed by an immunosuppressant [cyclophosphamide, cyclosporine, and IVIG (Synchronized immunosuppression therapy)] was reported to transiently reduce electrophysiologic abnormalities at the neuromuscular junction of some ALS patients [133].…”

Section: Immunosuppressive Therapy In Alsmentioning

confidence: 99%

“…Third, the observation that the IgG purified from a group of sporadic ALS patients, but not familial ALS patients, specifically interacts with the presynaptic membrane of motoneurons and modulates synaptic transmission through specific mechanisms also suggests that ALS-Abs can be pathogenic [18]. Fourth, a major concern is that the therapeutic approaches have failed [7–12]. However, it is likely that these immunosuppressive therapies were not appropriate.…”

Section: Autoimmunity As Pathogenic Mechanism In Alsmentioning

confidence: 99%

“…The remaining 90% is called sporadic ALS and does not show any conventional hereditary pattern. Similar efforts have been done searching for a therapeutic strategy without success [7–13]. To date, the pathogenic mechanisms of ALS continue being unknown.…”

Section: Introductionmentioning

confidence: 99%

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Autoimmunity in Amyotrophic Lateral Sclerosis: Past and Present

Pagani

González

Uchitel

2011

Neurology Research International

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting particularly motor neurons for which no cure or effective treatment is available. Although the cause of ALS remains unknown, accumulative evidence suggests an autoimmune mechanism of pathogenesis. In this paper, we will summarize the current research related to autoimmunity in the sporadic form of ALS and discuss the potential underlying pathogenic mechanisms and perspectives. Presented data supports the view that humoral immune responses against motor nerve terminals can initiate a series of physiological changes leading to alteration of calcium homeostasis. In turn, loss of calcium homeostasis may induce neuronal death through apoptotic signaling pathways. Additional approaches identifying specific molecular features of this hypothesis are required, which will hopefully allow us to develop techniques of early diagnosis and effective therapies.

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Section: Immunosuppressive Therapy In Alsmentioning

confidence: 99%

Section: Autoimmunity As Pathogenic Mechanism In Alsmentioning

confidence: 99%

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Autoimmunity in Amyotrophic Lateral Sclerosis: Past and Present

Pagani

González

Uchitel

2011

Neurology Research International

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“…Likewise, the recent identification of loss-of-function mutations in TBK1, a well-characterized regulator of innate immunity, as a cause of ALS/FTD (18,129,130) further reinforces the concept that immune dysregulation might be a characteristic feature of the disease. Despite the strong case for a connection between ALS/FTD and autoimmunity, there is also convincing evidence against the idea that ALS is itself a classical autoimmune condition, given that administration of immunosuppressive drugs including corticosteroids, azathioprine, and cyclophosphamide (alone or in combination), as well as plasmapheresis or intravenous Igs (IVIGs), has failed to alter the progression of the disease (131)(132)(133)(134)(135)(136)(137). Several reasons have been posited to explain the failure of these drugs to slow disease progression in ALS patients.…”

Section: R E V I E W S E R I E S : G L I a A N D N E U R O D E G E N mentioning

confidence: 99%

Microglia and C9orf72 in neuroinflammation and ALS and frontotemporal dementia

Lall¹,

Baloh²

2017

Journal of Clinical Investigation

142

102

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Genetic connections between microglia and neurodegenerationMicroglia are the main cells in the CNS responsible for immune surveillance and are critical for normal development and homeostasis (34)(35)(36). Under steady-state conditions, "ramified" microglia continuously survey the local microenvironment for any foreign antigens and insults. The resident microglia are Amyotrophic lateral sclerosis (ALS) is a degenerative disorder that is characterized by loss of motor neurons and shows clinical, pathological, and genetic overlap with frontotemporal dementia (FTD). Activated microglia are a universal feature of ALS/FTD pathology; however, their role in disease pathogenesis remains incompletely understood. The recent discovery that ORF 72 on chromosome 9 (C9orf72), the gene most commonly mutated in ALS/FTD, has an important role in myeloid cells opened the possibility that altered microglial function plays an active role in disease. This Review highlights the contribution of microglia to ALS/FTD pathogenesis, discusses the connection between autoimmunity and ALS/FTD, and explores the possibility that C9orf72 and other ALS/FTD genes may have a "dual effect" on both neuronal and myeloid cell function that could explain a shared propensity for altered systemic immunity and neurodegeneration.

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“…Multiple immunosuppressive drugs have been studied, including corticosteroids, plasmapheresis, intravenous immunoglobulin, cyclophosphamide, and cyclosporine, all of which failed to alter disease progression. [68][69][70][71][72] Minocycline is a tetracycline antibiotic that decreases inflammation by inhibiting microglial activation. 73 SOD1 animal studies were optimistic, showing delayed disease onset, prolonged survival, and decreased motor neuron loss when given to presymptomatic animals.…”

Section: Immunosuppressive Drugs and Proceduresmentioning

confidence: 99%

Amyotrophic Lateral Sclerosis: Drug Therapy from the Bench to the Bedside

Gibson

Bromberg

2012

Semin Neurol

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Amyotrophic lateral sclerosis (ALS) is an unrelenting progressive neurodegenerative disease causing progressive weakness, ultimately leading to death. Despite aggressive research, the pathways leading to neuronal death are incompletely understood. Riluzole is the only drug clinically proven to enhance survival of ALS patients, but its mechanism of action is not clearly understood. In this article, the proposed pathophysiology of ALS is reviewed including glutamate excitotoxicity, oxidative stress, mitochondrial dysfunction, autoimmune mechanisms, protein aggregation, SOD1 accumulation, and neuronal death. Based on these mechanisms, past major ALS drug studies will be reviewed as well as promising current ALS drug studies, focusing on the advancement of these studies from the bench to the patient's bedside.

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Results of Treatment of Certain Diseases of the Central Nervous System With Acth and Corticosteroids

Cited by 8 publications

References 12 publications

Autoimmunity in Amyotrophic Lateral Sclerosis: Past and Present

Autoimmunity in Amyotrophic Lateral Sclerosis: Past and Present

Microglia and C9orf72 in neuroinflammation and ALS and frontotemporal dementia

Amyotrophic Lateral Sclerosis: Drug Therapy from the Bench to the Bedside

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