Pathogenesis of vascular dementia in stroke-prone spontaneously hypertensive rats

Kimura, Shin-ichi; Saito, Hideya; Minami, Masaru; Togashi, Hiroko; Nakamura, Nishio; Nemoto, M.; Parvez, H.

doi:10.1016/s0300-483x(00)00312-7

Cited by 94 publications

(50 citation statements)

References 14 publications

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“…Complex interactions in producing cognitive decline have been shown (Fein et al, 2000) and changes in cortex and hippocampus, while other interactions suggested significant correlations between cortical lesions and frontal atrophy (Burton et al, 2003;Hentschel et al, 2003). Preclinical (Kimura et al, 2000) and clinical evidence (Swartz and Black, 2002) indicate that a cholinergic deficit similar to that seen in Alzheimer's dementia (AD) may be associated with vascular dementia (VaD); which suggests that these patients may benefit from treatment with cholinesterase inhibitors, as has been confirmed in recent studies (Erkinjuntti et al, 2000).…”

Section: Introductionmentioning

confidence: 89%

Vascular damage and EEG markers in subjects with mild cognitive impairment

Moretti

Miniussi

Frisoni

et al. 2007

Clinical Neurophysiology

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Objective: We evaluated the changes induced by cerebrovascular (CV) damage on brain rhythmicity recorded by electroencephalography (EEG) in a cohort of subjects with mild cognitive impairment (MCI). Methods: We enrolled 99 MCI subjects (Mini-Mental State Examination [MMSE] mean score 26.6). All subjects underwent EEG recording and magnetic resonance imaging (MRI). EEGs were recorded at rest. Individual EEG frequencies were indexed by the h/a transition frequency (TF) and by the individual a frequency (IAF) with power peak in the extended a range (5-14 Hz). Relative power was separately computed for d, h, a1, a2, and a3 frequency bands on the basis of the TF and IAF values. Subsequently, we divided the cohort in four sub-groups based on subcortical CV damage as scored by the age-related white matter changes scale (ARWMC). Results: CV damage was associated with 'slowing' of TF proportional to its severity. In the spectral bandpower the severity of vascular damage was associated with increased d power and decreased a2 power. No association of vascular damage was observed with IAF and a3 power. Moreover, the h/a1 ratio could be a reliable index for the estimation of the individual extent of CV damage. Conclusions: EEG analysis may show physiological markers sensitive to CV damage. The appropriate use of this EEG index may help the differential diagnosis of different forms of cognitive decline, namely primary degenerative and secondary to CV damage. Significance: The EEG neurophysiological approach, together with anatomical features from imaging, could be helpful in the understanding of the functional substrate of dementing disorders.

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Section: Introductionmentioning

confidence: 89%

Vascular damage and EEG markers in subjects with mild cognitive impairment

Moretti

Miniussi

Frisoni

et al. 2007

Clinical Neurophysiology

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“…White matter lesions may directly affect cholinergic projection [39,40], and preclinical [41,42] and clinical evidence [23,43] suggest that the cholinergic system might also be involved in VaD. Moreover, a severe cholinergic deficit in frontal and temporal cortices has been shown to occur in CADASIL cases [44,45].…”

Section: Vascular Dementia and Transcranial Magnetic Stimulation: An mentioning

confidence: 99%

A Review of Transcranial Magnetic Stimulation in Vascular Dementia

Pennisi

Ferri

Cantone

et al. 2011

Dement Geriatr Cogn Disord

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Vascular dementia (VaD) is a clinical syndrome that encompasses a wide spectrum of cognitive disorders caused by cerebrovascular disease. The subcortical ischemic form of VaD is clinically homogeneous and a major cause of cognitive impairment in the elderly. Vascular lesions contribute to cognitive decline in neurodegenerative dementias, and VaD and Alzheimer’s disease often coexist and share clinical features and multiple neurotransmission involvement. These similarities have led several investigators to use transcranial magnetic stimulation (TMS) to enucleate a neurophysiological profile of VaD. TMS studies have identified a pattern of cortical hyperexcitability probably related to the disruption of the integrity of white matter lesions due to cerebrovascular disease. The present review provides a perspective of these TMS techniques by further understanding the role of different neurotransmission pathways and plastic remodeling of neuronal networks in the pathogenesis of VaD.

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“…Fourth, rats with multiple small embolizations have been shown to produce multiple infarctions and exhibit decreases in cholinergic markers [19] . Finally, there is a significant reduction in cholinergic markers, including ACh, in the neocortex, hippocampus and cerebrospinal fluid (CSF) in the spontaneously hypertensive stroke prone rat (SHspR), which is the best model for essential hypertension and stroke [20,21] . It has been suggested that patients with VaD also exhibit cholinergic deficits (reviewed in ref [22] ).…”

Section: Cholinergic Deficiency In Vad Animal Models and Vad Patientsmentioning

confidence: 99%

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

2009

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Vascular dementia (VaD) is a progressive neurodegenerative disease with a high prevalence. Several studies have recently reported that VaD patients present cholinergic deficits in the brain and cerebrospinal fluid (CSF) that may be closely related to the pathophysiology of cognitive impairment. Moreover, cholinergic therapies have shown promising effects on cognitive improvement in VaD patients. The precise mechanisms of these cholinergic agents are currently not fully understood; however, accumulating evidence indicates that these drugs may act through the cholinergic anti-inflammatory pathway, in which the efferent vagus nerve signals suppress pro-inflammatory cytokine release and inhibit inflammation, although regulation of oxidative stress and energy metabolism, alleviation of apoptosis may also be involved. In this paper, we provide a brief overview of the cholinergic treatment strategy for VaD and its relevant mechanisms of anti-inflammation.

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Pathogenesis of vascular dementia in stroke-prone spontaneously hypertensive rats

Cited by 94 publications

References 14 publications

Vascular damage and EEG markers in subjects with mild cognitive impairment

Vascular damage and EEG markers in subjects with mild cognitive impairment

A Review of Transcranial Magnetic Stimulation in Vascular Dementia

Cholinergic deficiency involved in vascular dementia: possible mechanism and strategy of treatment

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