Neuroprotection in vascular dementia: A future path

Skoog, Ingmar; Korczyn, Amos D.; Guekht, Alla

doi:10.1016/j.jns.2012.02.013

Cited by 34 publications

(28 citation statements)

References 36 publications

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“…The Cochrane review stated that cerebrolysin may have positive effects on both cognitive and global functioning in elderly patients with VaD of mild to moderate severity [65–67]. Actovegin, a deproteinized ultrafiltrate of calf blood comprising more than 200 bioactive constituents, exhibits a range of pleiotropic neuroprotective and metabolic effects [68–70]; a study in a rat model of transient global cerebral ischemia found that it improved spatial learning and memory [70]. The recently completed ARTEMIDA study showed that actovegin (2000 mg i.v.…”

Section: Methodsmentioning

confidence: 99%

Towards the concept of disease-modifier in post-stroke or vascular cognitive impairment: a consensus report

Bordet

Ihl

Korczyn

et al. 2017

BMC Med

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BackgroundVascular cognitive impairment (VCI) is a complex spectrum encompassing post-stroke cognitive impairment (PSCI) and small vessel disease-related cognitive impairment. Despite the growing health, social, and economic burden of VCI, to date, no specific treatment is available, prompting the introduction of the concept of a disease modifier.Consensus and suggestionsWithin this clinical spectrum, VCI and PSCI remain advancing conditions as neurodegenerative diseases with progression of both vascular and degenerative lesions accounting for cognitive decline. Disease-modifying strategies should integrate both pharmacological and non-pharmacological multimodal approaches, with pleiotropic effects targeting (1) endothelial and brain–blood barrier dysfunction; (2) neuronal death and axonal loss; (3) cerebral plasticity and compensatory mechanisms; and (4) degenerative-related protein misfolding. Moreover, pharmacological and non-pharmacological treatment in PSCI or VCI requires valid study designs clearly stating the definition of basic methodological issues, such as the instruments that should be used to measure eventual changes, the biomarker-based stratification of participants to be investigated, and statistical tests, as well as the inclusion and exclusion criteria that should be applied.ConclusionA consensus emerged to propose the development of a disease-modifying strategy in VCI and PSCI based on pleiotropic pharmacological and non-pharmacological approaches.

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Section: Methodsmentioning

confidence: 99%

Towards the concept of disease-modifier in post-stroke or vascular cognitive impairment: a consensus report

Bordet

Ihl

Korczyn

et al. 2017

BMC Med

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“…In addition, the ARTEMIDA study explored whether this treatment has a disease-modifying effect on PSD [123]. Actovegin has been shown to have effects on some cellular processes in the aging brain and recent experimental studies revealed actovegin to play a role in neuroprotective mechanisms [124]. …”

Section: Lifestyle Interventionsmentioning

confidence: 99%

Post-stroke dementia – a comprehensive review

Mijajlović

Pavlović

Brainin

et al. 2017

BMC Med

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536

411

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Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing.

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“…There is some evidence that it may also be neuroprotective [56]. In a study of 200 patients with mild to moderate dementia, oral Actovegin Ò significantly improved the Syndrom Kurz Test and the Clinical Global Impression Scale scores versus placebo [57]. Recently, the ARTEMIDA (Actovegin in Patients with Post-Stroke Cognitive Impairment) study has been completed (n = 500) (Clinicaltrials.gov identifier NCT01582854 [59]), but the results are not available yet [56].…”

Section: Actovegin òmentioning

confidence: 99%

Pharmacotherapy to Enhance Cognitive and Motor Recovery Following Stroke

Beristaín

Golombievski

2015

Drugs Aging

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Stroke is a leading cause of disability among older adults and more than half of stroke survivors have some residual neurological impairment. Traditionally, managing the aftermath of stroke has been by the implementation of several physical and language therapy modalities. The limitations of these rehabilitation efforts have sparked an interest in finding other ways to enhance neurological recovery. Some of these novel approaches have included pharmacological interventions, cell-derived treatments, and cortical magnetic stimulation. Mounting evidence over the last 2 decades suggests that pharmacological manipulations may have the potential to modulate practice-dependent neuroplasticity and potentially improve neurological recovery after stroke. Multiple pharmacological agents with different mechanisms of action have been evaluated, showing conflicting results. Some studies suggest some promise, yet the quality of the available studies is suboptimal overall, with most of the studies being underpowered. So far, the most promising agents include the antidepressants for motor recovery and acetylcholinesterase inhibitors and memantine for aphasia. However, large, well-designed clinical trials are needed to address the shortcomings of the available data and before any pharmacological agent can be recommended for routine use as part of the standard algorithm of stroke management.

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Neuroprotection in vascular dementia: A future path

Cited by 34 publications

References 36 publications

Towards the concept of disease-modifier in post-stroke or vascular cognitive impairment: a consensus report

Towards the concept of disease-modifier in post-stroke or vascular cognitive impairment: a consensus report

Post-stroke dementia – a comprehensive review

Pharmacotherapy to Enhance Cognitive and Motor Recovery Following Stroke

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