Subcortical Vascular Dementia Research Articles

Cerebellar Atrophy in Patients with Subcortical-Type Vascular Cognitive Impairment

Recent studies suggest that the role of the cerebellum extends into cognitive regulation and that subcortical vascular dementia (SVaD) can result in cerebellar atrophy. However, there has been no evaluation of the cerebellar volume in the preclinical stage of SVaD. We aimed to compare cerebellar volume among patients with amnestic mild cognitive impairment (aMCI) and subcortical vascular mild cognitive impairment (svMCI) and evaluate which factors could have contributed to the cerebellar volume. Participants were composed of 355 patients with aMCI, svMCI, Alzheimer's disease (AD), and SVaD. Cerebellar volumes were measured using automated methods. A direct comparison of the cerebellar volume in SVaD and AD groups showed that the SVaD group had a statistically smaller cerebellar volume than the AD group. Additionally, the svMCI group had a smaller cerebellar volume than the aMCI group, with the number of lacunes (especially in the supratentorial regions) being associated with cerebellar volume. Cerebellar volumes were associated with some neuropsychological tests, digit span backward and ideomotor apraxia. These findings suggest that cerebellar atrophy may be useful in differentiating subtypes of dementia and the cerebellum plays a potential role in cognition.

Amyloid Burdens in MCI of Alzheimer's Disease Versus Subcortical Vascular Dementia (S34.004)

Objective: We aimed to compare amyloid burden between patients with amnestic MCI (aMCI) and subcortical vascular MCI(svMCI). Background Most studies on mild cognitive impairment (MCI) have been focused on aMCI which is the preclinical stage of Alzheimer9s disease (AD). In contrast, only a few studies have involved patients in the preclinical stages of subcortical vascular dementia(svMCI). A recent study using Pittsburg compound-B (PiB) PET suggested that over 30% of patients who had been clinically diagnosed with SVaD showed significant amyloid deposits. However, to our knowledge, there has been no study investigating amyloid burden in patients with svMCI. We aimed to compare amyloid burden between patients with aMCI and svMCI, and to evaluate the effects of amyloid burden on cognition in patients with svMCI. Design/Methods: Participants consisted of 45 aMCI and 67 svMCI patients. All aMCI patients met Petersen9s criteria and all svMCI patients met Petersen9s criteria with some modifications that were previously described. Patients with svMCI had extensive white matter hyperintensities (WMH). All the patients underwent 3.0T MRI, 11C-Pittsburgh compound B (PiB) PET and detailed neuropsychological testing. Results: Twenty eight (62.2%) of the 45 patients with aMCI were positive PiB (PiB(+)), while twenty two (32.8%) of the 67 patients with svMCI were PiB(+). The mean uptake ratio of PiB was higher in aMCI (1.868 ± 0.512) than svMCI (1.504±0.402) (p Conclusions: Our findings suggested that patients with svMCI showed lower amyloid burdens than aMCI. We also found that amyloid burden affected memory dysfunction in patients with svMCI. Disclosure: Dr. Lee has nothing to disclose. Dr. Seo has nothing to disclose. Dr. Na has nothing to disclose.

The value of diffusion tensor imaging in the differential diagnosis of subcortical ischemic vascular dementia and Alzheimer's disease in patients with only mild white matter alterations on T2-weighted images

Diffusion tensor imaging (DTI) is a form of functional magnetic resonance imaging (MRI) that allows examination of the microstructural integrity of white matter in the brain. Dementia is a neurodegenerative disease, and DTI can provide indirect insights of the microstructural characteristics of brains in individuals with different forms of dementia. To evaluate the value of DTI in the diagnosis and differential diagnosis of patients with subcortical ischemic vascular dementia (SIVD) and Alzheimer's disease (AD). The study included 40 patients (20 AD patients and 20 SIVD patients) and 20 normal controls (NC). After routine MRI and DTI, fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values were measured and compared in regions of interest (ROI). Compared to NC and AD patients, SIVD patients had lower FA values and higher ADC values in the inferior-fronto-occipital fascicles (IFOF), genu of the corpus callosum (GCC), splenium of the corpus callosum (SCC), and superior longitudinal fasciculus (SLF). Compared to controls and SIVD patients, AD patients had lower FA values in the anterior frontal lobe, temporal lobe, hippocampus, IFOF, GCC, and CF; and higher ADC values in the temporal lobe and hippocampus. DTI can be used to estimate the white matter impairment in dementia patients. There were significant regional reductions of FA values and heightened ADC values in multiple regions in SIVD patients compared to AD patients. When compared with conventional MRI, DTI may provide a more objective method for the differential diagnosis of SIVD and AD disease patients who have only mild white matter alterations on T2-weighted imaging.

Cardiovascular Risk Factors Cause Cortical Thinning in Cognitively Impaired Patients

Cardiovascular risk factors are associated with cognitive impairments. However, the effects of cardiovascular risk factors on the topography of cortical thinning have not yet been studied in patients with mild cognitive impairment (MCI) or dementia. Thus, we aimed to evaluate the topography of cortical thinning related to cardiovascular risk factors and the relationships among cardiovascular risk factors, white matter hyperintensities (WMH), and cortical atrophy. Participants included 226 patients with Alzheimer disease or subcortical vascular dementia and 135 patients with amnestic MCI or subcortical vascular MCI. We automatically measured the volume of WMH and cortical thickness. Hypertension was associated with cortical thinning in the frontal and perisylvian regions, and cortical thinning related to diabetes mellitus (DM) occurred in the frontal region. In path analyses, hypertension accounted for 0.04 of the frontal thinning with the mediation of WMH and 0.16 without the mediation of WMH. In case of DM, it accounted for 0.02 of the frontal thinning with the mediation of WMH and 0.13 without the mediation of WMH. Hypertension and DM predominantly affected frontal thinning both with and without the mediation of WMH, where the effects without the mediation of WMH were greater than those with the mediation of WMH.

The Profile of Hippocampal Metabolites Differs between Alzheimer's Disease and Subcortical Ischemic Vascular Dementia, as Measured by Proton Magnetic Resonance Spectroscopy

Alzheimer's disease (AD) and subcortical ischemic vascular dementia (SIVD) have overlapping pathologies and risk factors, but their underlying neurodegenerative mechanisms are basically different. We performed magnetic resonance spectroscopy (MRS) to study metabolite differences between the two diseases in vivo. The subjects were 31 patients with SIVD and 99 with AD. Additionally, 45 elderly subjects were recruited as controls. We measured N-acetylaspartate (NAA), glutamine and glutamate (Glx), and myoinositol (mIns) concentration quantitatively using a 1.5-T MR scanner. N-acetylaspartate and Glx concentrations decreased in the hippocampus and cingulate/precuneal cortices (PCC) in both AD and SIVD patients, and the NAA decrease in the hippocampus was more prominent in AD than in SIVD. Interestingly, the pattern of mIns concentration changes differed between the two disorders; mIns was increased in AD but not increased in SIVD. If one differentiates between AD and SIVD by the mIns concentration in the hippocampus, the area under the receiver operating characteristic curve was 0.95, suggesting a high potential for discrimination. Our results suggest that proton MRS can provide useful information to differentiate between AD and SIVD. The difference of mIns concentrations in the hippocampus and PCC seems to reflect the different neurodegenerative mechanisms of the two disorders.

Abstract 2986: Bilateral Thalamic Lesions in Subcortical Vascular Dementia

Subcortical vascular dementia (SVaD) is categorized to the group of dementia due to the small-vessel disease which consists of lacunar infarcts, microbleeds and leuko-araiosis. However, the causative lesions and their relationship have not been clarified yet in SVaD. In order to elucidate the pathophysiology underlying SVaD, MR findings and vascular risk factors were analyzed in 31 patients (25 men and 6 women) who were diagnosed as having SVaD based on the NINDS-AIREN criteria. Their mean age was 75.7 years. Thirty-six non-demented patients with asymptomatic cerebral infarction (ACI) and 49 non-demented patients with symptomatic lacunar infarcts (SCI) served as disease controls. All subjects underwent 1.5 Tesla MRI including T1WI, T2WI, T2*WI, FLAIR and MR angiography. Numbers of lacunar infarcts and old microbleeds were counted in all MR slices, and the degree of leuko-araiosis was evaluated according the Fazekas’ categories. Laboratory studies included fibrinogen, d-dimer, serum lipid profile, glucose, plasma immunoreactive insulin (IRI) and brain natriuretic peptide (BNP). In the neuropsychological evaluation, MMSE, clock drawing test (CDT) and Benton’s visual retention test (BVRT) were carried out. In the results, the mean MMSE score was 13.0, and the mean CDT was 2.7/5.0. In the MR findings, the mean number of lacunar infarcts was 11.4, 15.2 and 17.2 for ACI, SCI and SVaD group, respectively. Thalamic lesions were detected in 30 (96.8%) of 31 SVaD patients, and 86.6% were lacunar infarcts whereas 13.3% were microbleeds on T2*WI. Bilateral thalamic lesions were detected in 66.7%, and the right-side and left-side lesions were seen in 16.6%, respectively. Antero-medial thalamic lesion was detected in 23.3%. No bilateral thalamic lesions were found in ACI or SCI group. Microbleeds were detected in 90% of SVaD patients. The mean number of microbleeds was 1.3, 2.1 and 5.8 for ACI, SCI and SVaD group, respectively. In the laboratory studies, the mean fibrinogen was significantly greater in SVaD group than in ACI or SCI group. The mean insulin was significantly greater in SVaD group than in ACI and SCI group. Advanced leuko-araiosis (Grade II and III) was seen in 87.1% of SVaD patients, whereas 52.8% of ACI patients and 34.7% of SCI patients. In the laboratory studies, the mean fibrinogen, IRI and BNP were significantly greater in SVaD group than in ACI or SCI group (p<0.05). The mean ratio of LDL-cholesterol to HDL-cholesterol was significantly greater in SVaD and SCI groups than in ACI group (p<0.05). In the present results, thalamic lesions, especially bilateral thalamic lesions, were detected frequently in SVaD patients. As thalamus plays an important role in both medial limbic and basolateral limbic systems which mediate cognitive information processing including memory and emotion, thalamic lesions may redound to the formation of SVaD.

Neurobehavioral Dysfunction in Patients with Subcortical Vascular Mild Cognitive Impairment and Subcortical Vascular Dementia

Amnestic mild cognitive impairment (MCI) is considered to be a prodromal stage of Alzheimer's disease. Likewise, subcortical vascular MCI (svMCI) is considered as a prodromal stage of subcortical vascular dementia (SVaD). The objective of this study was to investigate neuropsychiatric features in patients with svMCI compared to healthy controls and patients with SVaD. We evaluated 31 patients with svMCI, 42 with SVaD, and 28 healthy controls who underwent neuropsychiatric assessments using the Neuropsychiatric Inventory (NPI) and the Frontal Behavioral Inventory (FBI). On both the NPI and FBI, SVaD patients had the most severe neuropsychiatric symptoms, followed by svMCI patients and then healthy controls, suggesting that svMCI might be a prodromal stage of SVaD in terms of neuropsychiatric abnormalities. When we compared the differences of mean scores between negative and positive symptoms in FBI, negative symptoms tended to be more predominant than positive symptoms in both svMCI and SVaD patients, but the tendency was stronger in SVaD patients than in svMCI patients. These results suggest that vascular cognitive impairment with small vessel disease would start with both negative and positive neuropsychiatric symptoms and progress to present more severe negative symptoms. These behavioral ratings may be useful for early detection of vascular cognitive impairment associated with small vessel disease.

Lack of Association between Apolipoprotein E Polymorphism with Age at Onset of Subcortical Vascular Dementia

Background and Purpose: The relationship between apolipoprotein E (ApoE) and onset of vascular dementia remains controversial. The aim of this study was to evaluate the relationship between ApoE polymorphism and the onset of subcortical vascular dementia (SVaD) compared to Alzheimer’s disease (AD) and normal controls. Methods: The study was comprised of 61 patients with SVaD (42 Binswanger type, 19 lacunar type) and 112 patients with AD (16 early-onset AD, 96 late-onset AD) as well as 284 age-, gender- and education-matched normal controls. The diagnosis of SVaD was based on modified NINDS-AIREN criteria, and the diagnosis of AD was based on NINCDS-ADRDA criteria. ApoE polymorphism was genotyped in all participants. Results: None of the three ApoE alleles was more prevalent in SVaD patients compared to normal controls, which was the case when both Binswanger and lacunar types were analyzed separately. ApoE Ε4 did not accelerate the onset of SVaD (OR 1.66, 95% CI: 0.8–3.4), in contrast to a significant relation with late-onset AD (OR 3.78, 95% CI: 2.2–6.5). Conclusion: Our results suggest that ApoE polymorphism is not associated with the onset of SVaD and that the two subtypes of SVaD may share similar pathophysiologies.

Risk and Determinants of Dementia in Patients with Mild Cognitive Impairment and Brain Subcortical Vascular Changes: A Study of Clinical, Neuroimaging, and Biological Markers—The VMCI-Tuscany Study: Rationale, Design, and Methodology

Dementia is one of the most disabling conditions. Alzheimer's disease and vascular dementia (VaD) are the most frequent causes. Subcortical VaD is consequent to deep-brain small vessel disease (SVD) and is the most frequent form of VaD. Its pathological hallmarks are ischemic white matter changes and lacunar infarcts. Degenerative and vascular changes often coexist, but mechanisms of interaction are incompletely understood. The term mild cognitive impairment defines a transitional state between normal ageing and dementia. Pre-dementia stages of VaD are also acknowledged (vascular mild cognitive impairment, VMCI). Progression relates mostly to the subcortical VaD type, but determinants of such transition are unknown. Variability of phenotypic expression is not fully explained by severity grade of lesions, as depicted by conventional MRI that is not sensitive to microstructural and metabolic alterations. Advanced neuroimaging techniques seem able to achieve this. Beside hypoperfusion, blood-brain-barrier dysfunction has been also demonstrated in subcortical VaD. The aim of the Vascular Mild Cognitive Impairment Tuscany Study is to expand knowledge about determinants of transition from mild cognitive impairment to dementia in patients with cerebral SVD. This paper summarizes the main aims and methodological aspects of this multicenter, ongoing, observational study enrolling patients affected by VMCI with SVD.

The “Closing-In” Phenomenon in Parkinson’s Disease Dementia and Lewy-Body Dementia

The “Closing-In” Phenomenon in Parkinson’s Disease Dementia and Lewy-Body Dementia

Micro-vascular Diseases of White Matter

White matter hyperintensity (WMH) is commonly observed on the brain MRI of elderly subjects. It has been considered as an important biomarker for the micro-vascular damages of white matter of the brain. Aging, hypertension, diabetes mellitus, and hyperhomocysteinemia have been associated with WMH development. WMH is an important risk factor for the vascular dementia (VD), however it also considered as one of risk factors for conversion of mild cognitive impairment to dementia and progression of Alzheimer’s disease (AD). WMH has impact on gait, bladder control, and fine motor coordination. It also has negative effects on memory retrieval, mental flexibility, mental processing speed, and executive function by disconnecting nerve fibers that convey signals for normal cognition. Control of vascular risk factors can delay progression of WMH and this may be beneficial for VD as well as AD with ischemic changes, especially in the early state of diseases. In this paper, we will review clinical significance of WMH and three important diseases, subcortical vascular dementia, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, and cerebral amyloid angiopathy that associated with cerebral micro-vascular damages. Received: September 21, 2012 Revision received: September 25, 2012 Accepted: September 25, 2012

Selective white matter abnormalities in a novel rat model of vascular dementia

Rats subjected to bilateral common carotid artery (CCA) occlusion or 2-vessel occlusion (2VO) have been used as animal models of subcortical ischemic vascular dementia. However, this model possesses an inherent limitation in that cerebral blood flow (CBF) drops too sharply and substantially after ligation of CCAs. To circumvent such hypoxic-ischemic conditions, we tested implantation of the ameroid constrictor device on bilateral CCAs of male Wistar-Kyoto rats and more precisely replicated chronic cerebral hypoperfusion by gradual narrowing of the CCAs (2-vessel gradual occlusion; 2VGO). The acute cerebral blood flow reduction and resultant inflammatory responses observed in the 2VO rats were eliminated in the 2VGO rats. Thus, chronic cerebral hypoperfusion was segregated, and induced selective white matter changes with relatively preserved neurovascular coupling and substantially less metabolic and histological derangements in the gray matter including the hippocampus. This led to significant spatial working memory impairment of a magnitude similar to the 2VO rats at 28 days postoperation. The 2VGO model may more closely mimic cognitive impairment subsequent to selective white matter damage.

Preservation of cortical histamine H3 receptors in ischemic vascular and mixed dementias

AimHistamine H3 receptor antagonists have been proposed as a novel therapeutic approach for the symptomatic treatment of Alzheimer's disease (AD). However, it is unclear whether there is a neurochemical basis for extending their potential use in vascular and mixed dementias. In this study, we measured cortical H3 receptors in patients with subcortical ischemic vascular dementia (SIVD) and mixed SIVD/AD (MIX). Materials and methodsRadioligand binding assays using [3H]GSK189254 were used to measure H3 receptors in the postmortem frontal cortex, anterior cingulate gyrus and hippocampus of a cohort of longitudinally assessed SIVD, MIX and age-matched controls. ResultsH3 receptor levels were unchanged in SIVD and MIX in all areas studied. Furthermore, frontal H3 receptor densities negatively correlated with predeath assessment of cognition using Mini-Mental State Examination (MMSE) scores. ConclusionOur data suggest that H3 receptors are preserved in SIVD and MIX, thus supporting further assessments of H3 antagonists as potential therapeutics in these dementias.

Neurologic signs in relation to cognitive function in subcortical ischemic vascular dementia: a CREDOS (Clinical Research Center for Dementia of South Korea) study

The objective of this study was to investigate the relationship between neurologic signs and cognitive dysfunction in subcortical ischemic vascular dementia (SIVD). 121 patients with SIVD were recruited from multiple nationwide hospitals. The patients' neurologic signs were evaluated using the Focal Neurologic Sign Score (FNSS). The FNSS scores did not correlate with the composite neuropsychology scores and Korean Mini-Mental State Examination scores. The FNSS scores correlated with the letter fluency and Rey-Osterrieth Complex Figure (ROCF) copy scores. Using a multivariate regression analysis controlled for age, sex, and educational level, the FNSS scores had a significant relationship with the letter fluency test scores (R (2) = 0.08, β = -2.28, p = 0.02) and ROCF copy scores (R (2) = 0.08, β = -0.42, p = 0.03). These findings suggest that the neurologic signs in patients with SIVD do not correlate with global cognitive functions; however, these signs do correlate with executive dysfunction in these patients.

Longitudinal changes of cortical morphology in CADASIL

In CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leucoencephalopathy), a genetic model of subcortical ischemic vascular dementia (SIVD), clinical status was previously found related to cortex morphology. In the present report, alterations of cortex morphology and their links to clinical worsening were investigated in 190 CADASIL patients followed during 24.4 months. Linear models were used to test relationships between: (1) clinical worsening and changes of depth of cortical sulci and of cortical thickness; (2) alterations of cortical morphology and changes of volume of white matter hyperintensities (WMHv) and of lacunar lesions (LLv). Reduction of sulcal depth was independently associated with increased time to complete trail making test A and B (p < 0.0001 and p = 0.004) and that of cortical thickness to increased disability (modified Rankin's scale, p = 0.008), while brain atrophy was only related to global cognitive worsening (Mattis dementia rating scale, p = 0.002). The impact of volume of lacunar lesions on cortical alterations was larger than that of volume of white matter hyperintensities. Cortical alterations, mainly related to lacunar lesions, evolve parallel to clinical worsening. These results further support the eventual role of cortical alterations in subcortical ischemic vascular dementia.

The Chinese (Cantonese) Montreal Cognitive Assessment in Patients with Subcortical Ischemic Vascular Dementia

Background: Subcortical ischemic vascular dementia (SIVD) has been proposed as the most frequent subtype of vascular cognitive impairment. The aim of this study was to evaluate the psychometric properties of the Chinese (Cantonese) Montreal Cognitive Assessment (CC- MoCA) in patients with SIVD in the Guangdong Province of China. Methods: 71 SIVD patients and 60 matched controls were recruited for the CC-MoCA, Mini Mental State Examination and executive clock drawing tasks. Receiver-operating characteristic curve analyses were performed to determine optimal sensitivity and specificity of the CC-MoCA total score in differentiating mild vascular dementia (VaD) patients from moderate VaD patients and controls. Results: The mean CC-MoCA scores of the controls, and mild and moderate VaD patients were 25.2 ± 3.8, 16.4 ± 3.7, and 10.0 ± 5.1, respectively. In our study, the optimal cutoff value for the CC-MoCA to be able to differentiate patients with mild VaD from controls is 21/22, and 13/14 to differentiate mild VaD from moderate VaD. Conclusion: The CC-MoCA is a useful cognitive screening instrument in SIVD patients.

Attenuation of Brain Damage and Cognitive Impairment by Direct Renin Inhibition in Mice With Chronic Cerebral Hypoperfusion

The role of the renin-angiotensin system in cognitive impairment is unclear. This work was undertaken to test our hypothesis that renin-angiotensin system may contribute to cognitive decline and brain damage caused by chronic cerebral ischemia. C57BL/6J mice were subjected to bilateral common carotid artery stenosis with microcoil to prepare mice with chronic cerebral hypoperfusion, a model of subcortical vascular dementia. The effects of aliskiren, a direct renin inhibitor, or Tempol, a superoxide scavenger, on brain damage and working memory in these mice were examined. Chronic cerebral hypoperfusion significantly increased brain renin activity and angiotensinogen expression in C57BL/6J mice, which was attributed to the increased renin in activated astrocytes and microvessels and the increased angiotensinogen in activated astrocytes in white matter. Aliskiren pretreatment significantly inhibited brain renin activity and ameliorated brain p67(phox)-related NADPH oxidase activity, oxidative stress, glial activation, white matter lesion, and spatial working memory deficits in C57BL/6J mice with bilateral common carotid artery stenosis. To elucidate the role of oxidative stress in brain protective effects of aliskiren, we also examined the effect of Tempol in the same mice with bilateral common carotid artery stenosis. Tempol pretreatment mimicked the brain protective effects of aliskiren in this mouse model. Posttreatment of mice with aliskiren or Tempol after bilateral common carotid artery stenosis also prevented cognitive decline. In conclusion, chronic cerebral hypoperfusion induced the activation of the brain renin-angiotensin system. Aliskiren ameliorated brain damage and working memory deficits in the model of chronic cerebral ischemia through the attenuation of oxidative stress. Thus, direct renin inhibition seems to be a promising therapeutic strategy for subcortical vascular dementia.

Enhanced motor cortex facilitation in patients with vascular cognitive impairment-no dementia

Data on Transcranial Magnetic Stimulation (TMS) derived measures of cortical excitability and intracortical circuits in age-related white matter changes are scarce. We aimed to assess early changes of motor cortex excitability in nondemented elderly patients with subcortical ischemic vascular disease (SVD). Ten SVD elderly and ten age-matched controls underwent paired-pulse TMS for the analysis of intracortical inhibition (ICI) and facilitation (ICF). All subjects performed neuropsychological assessment and brain magnetic resonance imaging. SVD patients showed abnormal executive control function. No statistically significant differences were found for resting motor threshold, cortical silent period between SVD patients and controls or between the two hemispheres, in patients. A significant enhancement of mean ICF was observed in SVD patients. This study provides the first evidence of functional changes in intracortical excitatory neuronal circuits in patients with SVD and clinical features of vascular cognitive impairment-no dementia. Further studies are required to evaluate whether the observed change of ICF might predict cognitive and/or motor impairment in a population at risk for subcortical vascular dementia.

Revised NIA-AA criteria for the diagnosis of Alzheimer's disease: a step forward but not yet ready for widespread clinical use

In clinical medicine, diagnostic criteria are not only useful everyday tools for the practicing physician, but also represent a conceptual concentrate of the understanding of the etiology and pathophysiology of diseases at a given point in time. Although different sets of diagnostic criteria for Alzheimer's disease (AD) have been developed, the most widely used and best validated by clinico-pathological study to date are the NINCDS-ADRDA (National Institute of Neurological and Communicative Disorders and Stroke – Alzheimer's Disease and Related Disorders Association) criteria which were published in 1984 (McKhann et al., 1984). These criteria are largely based on the exclusion of other conditions that may cause dementia and can be succinctly but fairly summarized as defining AD as an “acquired progressive cognitive, behavioral, and functional impairment with no other obvious cause”. Clearly, the NINCDS-ADRDA criteria were etiology- and pathophysiology-agnostic in that they failed to point at any specific etiology, not even a degenerative one. They were also developed before other important causes of dementia, such as dementia with Lewy bodies, fronto-temporal dementia and subcortical vascular dementia had been fully described and characterized. The recent publication of a substantially revised version of these criteria (Sperling et al. 2011; Albert et al., 2011; McKhann et al., 2011), heralded by a largely European initiative four years ago (Dubois et al., 2007) has been greeted with great interest by the field. The newly proposed criteria reflect the substantial insights on disease pathophysiology gained over the last decades, especially regarding the molecular pathology of AD and the time course of such pathology in relation to clinical symptoms and disease.

Comparison between Alzheimer's Disease and Subcortical Vascular Dementia: Attentional Cortex Study in Functional Magnetic Resonance Imaging

Blood oxygen level dependent functional magnetic resonance imaging (fMRI) and the Stroop test were used to assess attentional cortex activation in patients with Alzheimer's disease, subcortical vascular dementia, and normal control subjects. Patients with Alzheimer's disease and subcortical vascular dementia demonstrated similar locations of cortical activation, including the bilateral middle and inferior frontal gyri, anterior cingulate and inferior parietal lobule in response to Stroop colour word stimuli. This activation was distinctly decreased in patients with dementia compared with normal control subjects. Different regions of the brain were activated in patients with Alzheimer's disease and subcortical vascular dementia compared with normal controls. fMRI is a useful tool for the study of dementia in humans and has some potential diagnostic value. Further studies with larger numbers of participants are required.