Cholinesterase inhibitors for Parkinson's disease: a systematic review and meta-analysis

Pagano, Gennaro; Rengo, Giuseppe; Pasqualetti, Giuseppe; Femminella, Grazia Daniela; Monzani, Fabio; Ferrara, Nicola; Tagliati, Michele

doi:10.1136/jnnp-2014-308764

Cited by 108 publications

(67 citation statements)

References 38 publications

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“…Some drug trials have indicated that their use could improve cognition among participants with Parkinson's disease dementia and dementia with Lewy bodies [29]. However, improved cognition in PD through the use of cholinesterase inhibitors can be accompanied by the increased tremor and adverse drug reactions [30]. …”

Section: Discussionmentioning

confidence: 99%

Mild cognitive impairment in Parkinson's disease versus Alzheimer's disease

Besser

Litvan

Monsell

et al. 2016

Parkinsonism & Related Disorders

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Introduction No known studies have compared longitudinal characteristics between individuals with incident mild cognitive impairment due to Parkinson's disease (PD-MCI) versus Alzheimer's Disease (AD-MCI). Methods We used longitudinal data from the National Alzheimer's Coordinating Center's Uniform Data Set to compare 41 PD-MCI and 191 AD-MCI participants according to their demographics, presence of ≥1 APOE e4 allele, and baseline and change over time in clinical characteristics, neuropsychological test scores, and Clinical Dementia Rating sum of boxes (CDR-SB). Multivariable linear regression models with generalized estimating equations were used to account for clustered data and to test for baseline and longitudinal differences in neuropsychological test scores. Results PD-MCI and AD-MCI participants differed by many demographic and clinical characteristics. Significantly fewer PD-MCI participants developed dementia over one year. Compared to AD-MCI participants, PD-MCI participants performed better at baseline and over time on a global measure of cognition (Mini Mental State Exam), memory measures (immediate and delayed Logical Memory), and a language measure (Boston Naming Test), and additionally performed better over time on an attention measure (Digit Span Forward), a language measure (Vegetable List), a processing speed measure (Digit Symbol), and an overall measure of memory and functional impairment (CDR-SB). Conclusion Our study provides further evidence that PD-MCI is clinically distinct from AD-MCI and requires different tools for diagnosis and monitoring clinical progression. More importantly, this study suggests that PD-MCI takes longer to convert into dementia than AD-MCI, findings that require replication by other studies.

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Section: Discussionmentioning

confidence: 99%

Mild cognitive impairment in Parkinson's disease versus Alzheimer's disease

Besser

Litvan

Monsell

et al. 2016

Parkinsonism & Related Disorders

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show abstract

“…A recent systematic review and meta-analysis suggested that AChE inhibitors are effective in the treatment of cognitive impairment in patients with PD. 120 The systematic search yielded three studies involving donepezil and one involving rivastigmine. Results showed that these drugs significantly slowed MMSE decline (MD=−1.123, 95% confidence interval (CI)=−1.638 to −0.608; P =0.001; I 2 =44.6%), and ADAS-cog (SMD=−0.266, 95% CI −0.399 to −0.133; P <0.0001; I 2 =0%).…”

Section: Cholinergic Disturbances In Pdmentioning

confidence: 99%

Deficits in cholinergic neurotransmission and their clinical correlates in Parkinson’s disease

Pérez-Lloret

Barrantes

2016

npj Parkinson's Disease

179

122

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In view of its ability to explain the most frequent motor symptoms of Parkinson’s Disease (PD), degeneration of dopaminergic neurons has been considered one of the disease’s main pathophysiological features. Several studies have shown that neurodegeneration also affects noradrenergic, serotoninergic, cholinergic and other monoaminergic neuronal populations. In this work, the characteristics of cholinergic deficits in PD and their clinical correlates are reviewed. Important neurophysiological processes at the root of several motor and cognitive functions remit to cholinergic neurotransmission at the synaptic, pathway, and circuital levels. The bulk of evidence highlights the link between cholinergic alterations and PD motor symptoms, gait dysfunction, levodopa-induced dyskinesias, cognitive deterioration, psychosis, sleep abnormalities, autonomic dysfunction, and altered olfactory function. The pathophysiology of these symptoms is related to alteration of the cholinergic tone in the striatum and/or to degeneration of cholinergic nuclei, most importantly the nucleus basalis magnocellularis and the pedunculopontine nucleus. Several results suggest the clinical usefulness of antimuscarinic drugs for treating PD motor symptoms and of inhibitors of the enzyme acetylcholinesterase for the treatment of dementia. Data also suggest that these inhibitors and pedunculopontine nucleus deep-brain stimulation might also be effective in preventing falls. Finally, several drugs acting on nicotinic receptors have proved efficacious for treating levodopa-induced dyskinesias and cognitive impairment and as neuroprotective agents in PD animal models. Results in human patients are still lacking.

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“…Cholinesterase inhibitors such as rivastigmine and donepezil can have a positive effect on cognitive function in PD, but may have a deleterious effect on motor function, particularly tremor. 18 Hallucinations can also respond to cholinesterase inhibitors. Quetiapine and clozapine are sometimes used to treat psychosis in PD; however, there is a lack of good evidence from controlled trials to support the use of quetiapine, and while there is better evidence to support the use of clozapine, physicians are often reluctant to use it as it is associated with haematological adverse events.…”

Section: Managing Cognitive and Psychiatric Aspectsmentioning

confidence: 99%