Acyclovir in Creutzfeldt-Jakob Disease

Newman, P.K.

doi:10.1016/s0140-6736(84)91302-3

Cited by 13 publications

(5 citation statements)

References 4 publications

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“…The initial designation of prion diseases as ‘slow viral illnesses’ led to the early evaluation of several antiviral treatments. Two case reports have been published on the use of acyclovir for the treatment of CJD [23,24]. Both cases were from the UK, female, and diagnosed as definite CJD.…”

Section: Human Prion Diseasesmentioning

confidence: 99%

Rapidly progressive dementias and the treatment of human prion diseases

Appleby

2010

Expert Opinion on Pharmacotherapy

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Importance of the field Rapidly progressive dementia (RPD) has many possible etiologies and definitive treatment is reliant upon an accurate diagnosis from an appropriate diagnostic work-up. A large portion of the neurodegenerative causes of RPD are due to prion diseases (e.g., Creutzfeldt–Jakob disease). The study of prion diseases, for which there is no currently available treatment, has public health implications and is becoming increasingly more relevant to our understanding of other protein misfolding disorders including Alzheimer’s disease, frontotemporal degeneration, and Parkinson’s disease. Areas covered in this review This article begins with an overview of the etiologies and diagnostic work-up of RPD followed by a detailed review of the literature concerning the treatment of human prion diseases (1971 to present). What the reader will gain The reader will understand the differential diagnosis and work-up of RPD as it pertains to its treatment, as well as an in-depth understanding of treatments of human prion diseases. Take home message An accurate diagnosis of the cause of RPD is of paramount importance when determining appropriate treatment. Most studies of the treatment for human prion diseases are case reports or case series, and results from only one randomized, placebo-controlled study have been reported in the literature (flupirtine). Studies have been hindered by disease heterogeneity and lack of standardized outcome measures. Although no effective prion disease treatment has been revealed through these studies, they provide important considerations for future studies.

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Section: Human Prion Diseasesmentioning

confidence: 99%

Rapidly progressive dementias and the treatment of human prion diseases

Appleby

2010

Expert Opinion on Pharmacotherapy

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“…Given that prion diseases were originally perceived as "slow virus" infections, it is no surprise that in early studies, acyclovir (264,265), vidarabine (266), interferon (267), and amantadine (268) were evaluated as potential prion therapies. Perhaps the best studied of these antivirals was amantadine, which demonstrated variegated responses in human trials (reviewed in reference 255).…”

Section: Antimicrobial Therapymentioning

confidence: 99%

Prions: Beyond a Single Protein

Das

Zou

2016

Clin Microbiol Rev

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SUMMARYSince the term protein was first coined in 1838 and protein was discovered to be the essential component of fibrin and albumin, all cellular proteins were presumed to play beneficial roles in plants and mammals. However, in 1967, Griffith proposed that proteins could be infectious pathogens and postulated their involvement in scrapie, a universally fatal transmissible spongiform encephalopathy in goats and sheep. Nevertheless, this novel hypothesis had not been evidenced until 1982, when Prusiner and coworkers purified infectious particles from scrapie-infected hamster brains and demonstrated that they consisted of a specific protein that he called a “prion.” Unprecedentedly, the infectious prion pathogen is actually derived from its endogenous cellular form in the central nervous system. Unlike other infectious agents, such as bacteria, viruses, and fungi, prions do not contain genetic materials such as DNA or RNA. The unique traits and genetic information of prions are believed to be encoded within the conformational structure and posttranslational modifications of the proteins. Remarkably, prion-like behavior has been recently observed in other cellular proteins—not only in pathogenic roles but also serving physiological functions. The significance of these fascinating developments in prion biology is far beyond the scope of a single cellular protein and its related disease.

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“…Acyclovir was unsuccessful in a case of early [243] and late [244]-onset treatment. Amantadine caused transient improvements in wakefulness and mentation in some patients [245,246], but no effects on survival were seen [247][248][249].…”

Section: Other Case Reportsmentioning

confidence: 99%