Association between amantadine and the onset of dementia in Parkinson's disease

Inzelberg, Rivka; Bonuccelli, Ubaldo; Schechtman, Edna; Miniowich, Ala; Strugatsky, Rosa; Ceravolo, Roberto; Logi, Chiara; Rossi, C. A.; Klein, Colin; Rabey, J. M.

doi:10.1002/mds.20968

Cited by 68 publications

(37 citation statements)

References 37 publications

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“…y-Axis, % of samples in that year containing these mutations; x-axis, year of sample collection. seasonal influenza viruses to patients with chronic neurological disorders (e.g., Parkinson's disease), who are on long-term, repeat prescriptions for amantadane [Luginger et al, 2000;Del Dotto et al, 2001;Thomas et al, 2004;Inzelberg et al, 2006;Reis et al, 2006]. Secondly, widespread, yet sporadic use of amantadane for the treatment of influenza may have contributed to the selection of adamantane-resistant viruses.…”

Section: Discussionmentioning

confidence: 99%

“…Amantadane has been used to treat dyskinesia in patients with Parkinson's disease [Luginger et al, 2000;Del Dotto et al, 2001;Thomas et al, 2004;Reis et al, 2006], as well as showing some benefits in delaying the onset of Parkinson's dementia [Inzelberg et al, 2006]. However, it was first investigated as an antiviral drug against influenza [Reis et al, 2006].…”

Section: Introductionmentioning

confidence: 99%

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Emergence of adamantane‐resistant influenza A(H3N2) viruses in Hong Kong between 1997 and 2006

Tang

Ngai

Wong

et al. 2008

Journal of Medical Virology

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Resistance to adamantanes for treating influenza A(H3N2) has increased dramatically, worldwide, over the past 5 years. A comprehensive 10-year data set on the rise of adamantane-resistance in Hong Kong is reported. Nucleotide sequences encoding the M2-ion channel of influenza A(H3N2) were obtained from 281 H3N2 isolates collected from adamantane-naive children admitted to a teaching hospital in Hong Kong, between 1997 and 2006. These sequences were screened for the presence of recognized adamantane resistance-associated amino acid mutations (L26F, V27A, A30T, S31N, G34E). The amantadane (rimantadine is not used in Hong Kong) usage for this hospital during this period was also collated. Fifty-eight isolates harbored at least one of these resistance signatures, the majority (57/58) being S31N, which increased rapidly over 2003-2005 from 20% to 83.3%. Other amino acid mutations, not previously associated with adamantane resistance, were also found. In particular, I51V was found to rise in frequency, along with S31N, though the significance of this mutation remains uncertain at present. A rise in amantadane usage occurred in Hong Kong between 2000 and 2002, which slightly preceded the subsequent rise in adamantane-resistant influenza A(H3N2) isolates. This study shows a temporal correlation between increases in amantadane prescriptions and the prevalence of adamantane-resistant influenza A(H3N2) viruses in Hong Kong. The underlying reasons for these findings are unclear and similar studies are required elsewhere to elucidate these and prevent this spread of drug-resistance happening again in future.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Emergence of adamantane‐resistant influenza A(H3N2) viruses in Hong Kong between 1997 and 2006

Tang

Ngai

Wong

et al. 2008

Journal of Medical Virology

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“…471 Another study found that amantadine may delay the onset of dementia in patients with PD, and attenuate its severity. 472 Chase and Oh 473 have proposed that amantadine might also have antidyskinetic effects because of its NMDA receptor antagonist property. They hypothesized that levodopa-induced pulsatile stimulation of dopamine receptors on MSNs induces abnormal phosphorylation of NMDA receptors leading to glutamate-mediated plastic changes and the development of motor complications.…”

Section: Modest Antiparkinsonian Effectmentioning

confidence: 99%

The scientific and clinical basis for the treatment of Parkinson disease (2009)

Olanow¹,

Stern²,

Sethi³

2009

Neurology

771

658

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Parkinson disease (PD) is an age-related neurodegenerative disorder that affects as many as 1-2% of persons aged 60 years and older. With the aging of the population, the frequency of PD is expected to increase dramatically in the coming decades. Current therapy is largely based on a dopamine replacement strategy, primarily using the dopamine precursor levodopa. However, chronic treatment is associated with the development of motor complications, and the disease is inexorably progressive. Further, advancing disease is associated with the emergence of features such as freezing, falling, and dementia which are not adequately controlled with dopaminergic therapies. Indeed, it is now appreciated that these nondopaminergic features are common and the major source of disability for patients with advanced disease. Many different therapeutic agents and treatment strategies have been evaluated over the past several years to try and address these unmet medical needs, and many promising approaches are currently being tested in the laboratory and in the clinic. As a result, there are now many new therapies and strategic approaches available for the treatment of the different stages of PD, with which the treating physician must be familiar in order to provide patients with optimal care. This monograph provides an overview of the management of PD patients, with an emphasis on pathophysiology, and the results of recent clinical trials. It is intended to provide physicians with an understanding of the different treatment options that are available for managing the different stages of the disease and the scientific rationale of the different approaches. 1 PD is the second most common neurodegenerative disorder, with an average age at onset of about 60 years. An estimated 5 million people throughout the world have PD, with 1 million individuals each in the United States and in Europe with the disorder. PD affects approximately 0.3% of the population and 1% to 2% of those older than 60 years.2 With the aging of the population and the substantial increase in the number of at-risk individuals older than 60 years, it is anticipated that the prevalence of PD will increase dramatically in the coming decades.

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“…Amantadine has been used for the treatment of Parkinsonism for more than 30 years and has been reported to influence longevity 23 and cognitive decline 24 in PD. In spite of its common use for gait disturbances, there are very few objective assessments of its effectiveness.…”

Section: Amantadinementioning

confidence: 99%

Medical treatment of freezing of gait

Giladi

2008

Mov. Disord.

131

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Freezing of gait (FOG) is frequently considered as one of the dopamine-resistant motor symptoms of Parkinsonism. Recent studies have clearly demonstrated that the Off-related FOG is improved by levodopa (L-dopa) or entacapone treatment. L-dopa can decrease duration of each FOG episode as well as its frequency. On-related FOGs are not common and difficult to diagnose. Only in the most advanced stages of the disease, FOGs are resistant to treatment as many other symptoms. Off-related FOGs are likely to be improved by dopamine agonists (DAs), but this has never been looked at systematically. In contrast, DA treatment might provoke FOG, and in two pivotal studies when DAs were compared to L-dopa in early stages of Parkinson's disease, the DA-treated arms experienced more FOGs. MAO-B inhibitors (selegiline and rasagiline) can decrease FOG frequency or severity, but its clinical significance is still unknown. L-Threo-DOPS has been reported to have a symptomatic beneficial effect in patients with pure freezing syndrome, but small-scale, controlled trials in Parkinson's disease could not support those early observations. Botulinum toxin injected into the calf muscles has been suggested to have a symptomatic benefit. However, double-blind, prospective studies could not support that early observation and increased fall risk in the injected patients has put this direction of treatment on hold. The potential benefit of amantadine, antidepressive drugs, acetylcholine esterase inhibitors, and methylphenidate on FOG has been studied in small-scale studies, and there is a need for prospective studies to understand the future role of those drugs.

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Association between amantadine and the onset of dementia in Parkinson's disease

Cited by 68 publications

References 37 publications

Emergence of adamantane‐resistant influenza A(H3N2) viruses in Hong Kong between 1997 and 2006

Emergence of adamantane‐resistant influenza A(H3N2) viruses in Hong Kong between 1997 and 2006

The scientific and clinical basis for the treatment of Parkinson disease (2009)

Medical treatment of freezing of gait

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