Purpose: Varenicline has demonstrated its safety and efficacy in Western studies including <3% of Asian participants. This prospective multi-center observational study investigated the safety and effectiveness of varenicline in Korean smokers. Patients and Methods: Smokers prescribed varenicline for the first time were enrolled from 252 medical institutions. Investigators recorded and graded all adverse events (AEs). To assess the effectiveness of varenicline, the 7-day point prevalence (PP) of smoking cessation was evaluated at the four visits during the 12-week treatment course. Rates of AE incidence and smoking cessation were analyzed using Chi-squared test or Fisher’s exact test. This study is registered with ClinicalTrials.gov, number NCT00483002. Results: A total of 3719 and 3700 study subjects were included in the safety and effectiveness analyses, respectively. Overall, 346 (9.3%) subjects experienced 471 AEs: 358 mild, 97 moderate, 9 severe, and 7 serious. The most frequent AEs were nausea (5.1%), dyspepsia (0.8%), abnormal dreams (0.8%), insomnia (0.8%), and headache (0.7%). Among the subjects with AEs, 73 subjects discontinued treatment, of which 68 were due to AE occurrence. The 7-day PP of smoking cessation at weeks 1–2, 3–6, 7–10, and ≥ week 11 were 51.7% (387/749), 59.6% (1740/2922), 73.3% (1114/1520), and 77.0% (1116/1449), respectively (p for trend = 0.023). Comorbidities and allergies were associated with a higher incidence of AEs and lower smoking cessation rate (p < 0.05). Younger subjects, infrequent alcohol drinkers, and lighter smokers showed a higher smoking cessation rate (p < 0.05). Conclusion: Varenicline in adult Korean smokers was well tolerated and effective as a smoking cessation aid in routine clinical practice.

Purpose: Varenicline has demonstrated its safety and efficacy in Western studies including <3% of Asian participants.This prospective multi-center observational study investigated the safety and effectiveness of varenicline in Korean smokers.Patients and Methods: Smokers prescribed varenicline for the first time were enrolled from 252 medical institutions.Investigators recorded and graded all adverse events (AEs).To assess the effectiveness of varenicline, the 7-day point prevalence (PP) of smoking cessation was evaluated at the four visits during the 12-week treatment course.Rates of AE incidence and smoking cessation were analyzed using Chi-squared test or Fisher's exact test.This study is registered with ClinicalTrials.gov,number NCT00483002.Results: A total of 3719 and 3700 study subjects were included in the safety and effectiveness analyses, respectively.Overall, 346 (9.3%) subjects experienced 471 AEs: 358 mild, 97 moderate, 9 severe, and 7 serious.The most frequent AEs were nausea (5.1%), dyspepsia (0.8%), abnormal dreams (0.8%), insomnia (0.8%), and headache (0.7%).Among the subjects with AEs, 73 subjects discontinued treatment, of which 68 were due to AE occurrence.The 7-day PP of smoking cessation at weeks 1-2, 3-6, 7-10, and ≥ week 11 were 51.7% (387/749), 59.6% (1740/2922), 73.3% (1114/1520), and 77.0%(1116/1449), respectively (p for trend = 0.023).Comorbidities and allergies were associated with a higher incidence of AEs and lower smoking cessation rate (p < 0.05).Younger subjects, infrequent alcohol drinkers, and lighter smokers showed a higher smoking cessation rate (p < 0.05).Conclusion: Varenicline in adult Korean smokers was well tolerated and effective as a smoking cessation aid in routine clinical practice.

Background: Recent advances in resting-state functional MRI have revealed altered functional networks in Alzheimer's disease (AD), especially those of the default mode network (DMN) and central executive network (CEN). However, few studies have evaluated whether small vessel disease (SVD) or combined amyloid and SVD burdens affect the DMN or CEN.Objective: The aim of this study was to evaluate whether SVD or combined amyloid and SVD burdens affect the DMN or CEN. Methods: In this cross-sectional study, we investigated the resting-state functional connectivity within DMN and CEN in 37 Pittsburgh compound-B (PiB)(+) AD, 37 PiB(-) subcortical vascular dementia (SVaD), 13 mixed dementia patients, and 65 normal controls.Results: When the resting-stateDMNof PiB(+) AD and PiB(-) SVaD patients were compared, the PiB(+) AD patients displayed lower functional connectivity in the inferior parietal lobule while the PiB(-) SVaDpatients displayed lower functional connectivity in the medial frontal and superior frontal gyri. Compared to the PiB(-) SVaD or PiB(+) AD, the mixed dementia patients displayed lower functional connectivity within the DMN in the posterior cingulate gyrus. When the resting- state CEN connectivity of PiB(+) AD and PiB(-) SVaD patients were compared, the PiB(-) SVaD patients displayed lower functional connectivity in the anterior insular region. Compared to the PiB(-) SVaD or PiB(+) AD, the mixed dementia patients displayed lower functional connectivity within the CEN in the inferior frontal gyrus.Conclusions: Our findings suggest that in PiB(+) AD and PiB(-) SVaD, there is divergent disruptions in resting-state DMN and CEN. Furthermore, patients with combined amyloid and SVD burdens exhibited more disrupted resting- state DMN and CEN than patients with only amyloid or SVD burden.

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.

Objectives: Despite many neuropsychological studies to differentiate subcortical vascular dementia (SVaD) from Alzheimer disease (AD), previous studies did not eliminate confounding effects of mixed Alzheimer and vascular pathology. We aimed to investigate neuropsychological differences between patients with Pittsburgh compound B (PiB)–negative SVaD and those with PiB-positive AD. Methods: We recruited patients who were clinically diagnosed with SVaD or AD and underwent an 11C-PiB-PET scan. All patients with SVaD fulfilled DSM-IV criteria for vascular dementia and had severe white matter hyperintensities. The diagnosis of AD was made on the basis of criteria for probable AD proposed by the National Institute of Neurological and Communicative Disorders and Stroke–Alzheimer’s Disease and Related Disorders Association. Results: The final patient sample consisted of 44/67 (65.7%) patients with SVaD who tested negative for PiB retention [PiB(−) SVaD] and 61/68 (89.7%) patients with AD who tested positive for PiB retention [PiB(+) AD]. Patients with PiB(−) SVaD performed better than patients with PiB(+) AD on both verbal and visual memory tests including delayed recalls of the Seoul Verbal Learning Test and Rey Complex Figure Test. Patients with PiB(−) SVaD were worse than patients with PiB(+) AD on phonemic fluency of the Controlled Oral Word Association Test and Stroop color test. Conclusions: Patients with PiB(−) SVaD were better at memory but worse at frontal function than patients with PiB(+) AD. The differences in memory/frontal functions observed between the 2 groups, however, could not differentiate all individual data due to some overlap in the cutoff threshold.

The "environmental dependency syndrome" refers to a loss of personal autonomy such that a person's environment almost entirely controls their actions. The goal of this study is to learn if patients with frontotemporal degeneration (FTD) exhibit prolonged TV watching, a behavior which may be a symptom of environmental dependency. We recruited 40 patients with FTD and 48 patients with Alzheimer's disease (AD), and asked these participants' caregivers about TV watching behaviors including total viewing time and channel/show preference, along with other behaviors indicative of environmental dependency. Compared to AD patients, FTD patients watched TV for a longer time. In addition, the patients who watched more TV showed more signs of environmental dependency. Increased TV watching may be a sign of environmental dependency, however further research is needed to explore other hypotheses.

Early-onset Alzheimer's disease (EOAD) has been shown to progress more rapidly than late-onset Alzheimer's disease (LOAD). However, no studies have compared the topography of brain volume reduction over time. The purpose of this 3-year longitudinal study was to compare EOAD and LOAD in terms of their rates of decline in cognitive testing and topography of cortical thinning. We prospectively recruited 36 patients with AD (14 EOAD and 22 LOAD) and 14 normal controls. All subjects were assessed with neuropsychological tests and with magnetic resonance imaging at baseline, Year 1, and Year 3. The EOAD group showed more rapid decline than the LOAD group in attention, language, and frontal-executive tests. The EOAD group also showed more rapid cortical thinning in widespread association cortices. In contrast, the LOAD group presented more rapid cortical thinning than the EOAD group only in the left parahippocampal gyrus. Our study suggests that patients with EOAD show more rapid cortical atrophy than patients with LOAD, which accounts for faster cognitive decline on neuropsychological tests.

Cerebrovascular disease (CVD) and amyloid burden are the most frequent pathologies in subjects with cognitive impairment. However, the relationship between CVD, amyloid burden, and cognition are largely unknown. We aimed to evaluate whether CVD (lacunes, white matter hyperintensities, and microbleeds) and amyloid burden (Pittsburgh compound B [PiB] retention ratio) contribute to cognitive impairment independently or interactively. We recruited 136 patients with subcortical vascular cognitive impairment who underwent magnetic resonance imaging, PiB–positron emission tomography, and neuropsychological testing. The number of lacunes was associated with memory, frontal dysfunctions, and disease severity. The volume of white matter hyperintensities and the PiB retention ratio were associated only with memory dysfunction. There was no direct correlation between CVD markers and PiB retention ratio except that the number of lacunes was negatively correlated with the PiB retention ratio. In addition, there were no interactive effects of CVD and PiB retention ratio on cognition. Our findings suggest that CVD and amyloid burden contribute independently and not interactively to specific patterns of cognitive dysfunction in patients with subcortical vascular cognitive impairment.

ObjectiveCerebral microbleeds (CMBs) are a neuroimaging marker of small vessel disease (SVD) with relevance for understanding disease mechanisms in cerebrovascular disease, cognitive impairment, and normal aging. It is hypothesized that lobar CMBs are due to cerebral amyloid angiopathy (CAA) and deep CMBs are due to subcortical ischemic SVD. We tested this hypothesis using structural magnetic resonance imaging (MRI) markers of subcortical SVD and in vivo imaging of amyloid in patients with cognitive impairment.MethodsWe included 226 patients: 89 with Alzheimer disease–related cognitive impairment (ADCI) and 137 with subcortical vascular cognitive impairment (SVCI). All subjects underwent amyloid imaging with [11C] Pittsburgh compound B (PiB) positron emission tomography, and MRI to detect CMBs and markers of subcortical SVD, including the volume of white matter hyperintensities (WMH) and the number of lacunes.ResultsParietal and occipital lobar CMBs counts were higher in PiB+ ADCI with moderate WMH than PiB+ ADCI with minimal WMH, whereas PiB− patients with SVCI (ie, “pure” SVCI) showed both lobar and deep CMBs. In multivariate analyses of the whole cohort, WMH volume and lacuna counts were positively associated with both lobar and deep CMBs, whereas amyloid burden (PiB) was only associated with lobar CMBs. There was an interaction between lacuna burden and PiB retention on lobar (but not deep) CMBs (p<0.001).InterpretationOur findings suggest that although deep CMBs are mainly linked to subcortical SVD, both subcortical SVD and amyloid‐related pathologies (eg, CAA) contribute to the pathogenesis of lobar CMBs, at least in subjects with mixed lobar and deep CMBs. Furthermore, subcortical SVD and amyloid‐related pathologies interact to increase the risk of lobar CMBs. Ann Neurol 2013;73:584–593

The Clinical Research Center for Dementia of South Korea (CREDOS) group developed a new classification system for ischemia using a combination of deep and periventricular white matter hyperintensities (WMHs). In this study, we aimed to evaluate the validity of the CREDOS ischemia classification system. A total of 352 patients with cognitive impairments were included. Their WMH scores were rated using the CREDOS WMH visual rating scale. These patients were divided into 3 groups according to the CREDOS ischemia classification system. The volume of WMH was also automatically measured. The number of lacunes and microbleeds (MBs) were counted. The CREDOS ischemia classification system was revised with factor analysis using vascular risk factors and cerebrovascular disease (CVD) markers (WMH volume, lacunes, and MBs). External validation was performed in another group of patients with cognitive impairment using multinomial logistic regression analysis. The CREDOS WMH visual rating scale showed excellent correlation with the automatically measured volume of WMH. The factor analysis showed that the severe group was expanded to D3P1 and D3P2 in the revised CREDOS ischemia classification system. In the validation group, the presence of vascular risk factors and the severity of CVD markers could be distinguished according to the revised CREDOS ischemia classification. We validated a newly developed classification system for ischemia. This simple visual classification system was capable of providing information on vascular risk factors and CVD markers by simply rating WMH on magnetic resonance imaging.

Objective: We hypothesized that early-onset Alzheimer9s disease(EOAD) has rapidly progressing cortical thinning and this cortical thinning may reveal a specific topography. Background Previous studies have shown that there are some differences between EOAD and late-onset Alzheimer9s disease(LOAD), however, the topographical difference of structural decline has not yet been reported longitudinally. Our 3 years longitudinal study investigated the rate of decline in neuropsychological tests and cortical thickness between EOAD and LOAD. Design/Methods: Thirty-six patients with Alzheimer9s disease(AD) to participate in the ADAPET study conducted by the Memory Disorder Clinic at Samsung Medical Center from March 2006 to December 2006 were included in this study. They fulfilled the criteria for probable AD proposed by the NINCDS-ADRDA. At the initial visit, all the patients underwent clinical interview, neurological examination, a battery of neuropsychological tests called the Seoul Neuropsychological Screening Battery (SNSB) and conventional brain MRI scans. Of the 36 patients, 27 patents completed annual follow-up over the course of 3 years. Results: Firstly, cognitive decline, EOAD had progressed rapidly over 3 years in terms of forward digit span, K-BNT, animals of COWAT, word reading of Stroop test and MMSE more than LOAD. Secondly, cortical thinning, when LOAD and EOAD groups were directly compared, EOAD showed more rapid cortical thinning in the left middle and inferior frontal gyrus, left inferior parietal lobule, posterior part of left superior temporal gyrus (Wernicke9s area), left fusiform gyrus, part of left cingulated gyrus, bilateral posterior cingulate gyri and precuneus. On the contrary, LOAD presented more rapid cortical thinning than EOAD group in Lt parahippocampal gyrus. Conclusions: Our longitudinal study demonstrates that EOAD shows more rapid cognitive and structural decline than LOAD. Particularly, the topography of structural decline was different between EOAD and LOAD. Disclosure: Dr. Cho has nothing to disclose. Dr. Jeon has nothing to disclose. Dr. Kim has nothing to disclose. Dr. Shin has nothing to disclose. Dr. Kim has nothing to disclose. Dr. Noh has nothing to disclose. Dr. Seo has nothing to disclose. Dr. Na has nothing to disclose.

Patients with early-onset Alzheimer's disease (EOAD) show more rapid progression, more generalized cognitive deficits and greater cortical atrophy and hypometabolism compared to patients with late-onset Alzheimer's disease (LOAD) at a similar disease stage. The purpose of this study was to compare the distribution and burden of fibrillar amyloid-ß between EOAD and LOAD in the two extremes classification. We evaluated 68 patients with AD (61 with PiB-positive (PiB+) and 7 with PiB-negative (PiB-)) who underwent brain MRI, Pittsburg compound-B (PiB) PET and detailed neuropsychological tests. Sixty-one patients with PiB+ AD were divided according to the age at onset: Seventeen patients belonged to EOAD group (age onset <60 years); 24 patients to LOAD group (onset age ≥70 years); the remaining is 20 patients (60 years ≤onset age < 70 years). This study analyzed between the two extremes (PiB+ EOAD vs LOAD group). Group differences in tracer uptake were assessed on a voxel-wise basis using statistical parametric mapping, and by comparing mean values in regions of interest. EOAD group showed significantly increased [11C]-labeled PiB uptake throughout bilateral basal ganglia, bilateral thalamus, left lateral temporal cortex and left occipital cortex on voxel-wise and region of interest comparisons (P<0.05). Our findings demonstrated that EOAD group has greater amyloid burden than LOAD group and there are consistent with postmortem pathologic studies.

Subcortical vascular cognitive impairment (SVCI) is characterized by white matter hyperintensities (WMH), lacunes, and microbleeds (MB) on brain MRI. A recent study showed that about 30% of clinically diagnosed patients with subcortical vascular dementia (SVaD) had significant amyloid burden as determined by Pittsburg compound-B (PiB)-PET. We evaluated the relationship between the three small vessel disease (SVD) MRI markers and PiB uptake and tested whether SVD markers and PiB uptake independently or synergistically contribute to cognitive impairment. We evaluated 136 patients with SVCI who underwent brain MRI, PiB-PET, and detailed neuropsychological tests. We performed multivariable regression modeling after controlling for possible confounders. Possible interactions between global cortical PiB uptake ratio and SVD markers were evaluated. SVD markers affected specific cognitive domains independent of PiB uptake. WMH influenced multiple cognitive impairments including language, visuospatial and memory functions, as well as frontal executive dysfunctions. Lacunes primarily affected frontal/executive and memory function. MB affected attention and visuospatial function. PiB uptake was also associated with language and verbal memory functions independent of SVD markers. There was no relationship between SVD markers and PiB uptake, and they do not interact in affecting cognition.

Patients with amnestic mild cognitive impairment (aMCI) are at increased risk of developing Alzheimer's disease. Fibrillar form amyloid deposition can be identified in vivo by Pittsburgh compound B (PIB) PET. According to the previous studies, a considerable proportion of aMCI patients are PIB negative. However, to our knowledge, few studies have elucidated the diagnostic entity of PIB negative aMCI (PNMCI). Cognitive performance, hippocampal shape, regional cortical thickness pattern, and functional connectivity were compared between 79 cognitively normal (NC), 31 PIB positive aMCI (PPMCI) and 17 PNMCI subjects. Functional connectivity across whole brain was examined by resting state functional MRI analysis using independent component analysis. PPMCI subjects had lower scores in visual and verbal memory tests but had higher scores in attention (digit span backward) test than PNMCI. Compared to NC, PPMCI showed cortical thinning in bilateral hippocampi, bilateral precuneus, and bilateral inferior parietal lobules, while PNMCI had thinning tendency in left anterior cingulate cortex and right hippocampus. No significant difference in regional cortical thinning pattern was observed between PPMCI and PNMCI. Hippocampal shape analyses revealed significant deformations of the bilateral hippocampi not only in PPMCI but also in PNMCI, when compared to NC. There were no differences of hippocampal deformation pattern between PNMCI and PPMCI. Lastly, PPMCI subjects had significantly decreased functional connectivity in the previously known DMN areas including bilateral posterior cingulate cortex, right medial temporal lobe, bilateral middle temporal gyri, and left superior temporal gyrus. On the other hand, PNMCI subjects showed significantly decreased functional connectivity in posterior portion of the left middle temporal gyrus, which was not a component of the previously known DMN area. Diabetes mellitus and hypertension were more common in PNMCI than PPMCI. With comparable and minimal amount of white matter hyperintensities, PNMCI had more lacunar infarction than PPMCI. Although PNMCI had hippocampal atrophy indistinguishable from PPMCI, functional connectivity and cortical thickness analysis revealed that PNMCI subjects have pathological substrates for their cognitive impairment other than AD. In this study, small vessel disease without severe white matter hyperintensity may be a probable suspect.

Resting state fMRI has shown distinct patterns of network disruption across the major neurodegenerative diseases. Specifically, recent studies have shown that patients with Alzheimer's disease (AD) have disruption in the areas of default mode network (DMN). Moreover, DMN largely overlap with high amyloid burden areas in AD, suggesting amyloid toxicity affects disconnection of DMN. Despite recent advance of our knowledge on functional connectivity, the relationships between subcortical ischemia and DMN connectivity has not been studied. Also, there were no studies evaluating the interactive effects of small vessel disease and amyloid burdens on DMN connectivity. Thus, we sought to compare DMN connectivity in Pittsburg compound-B (PiB) (+) AD, PiB (-) and PiB (+) subcortical vascular dementia (SVaD). We recruited 39 patients with PIB(+) AD, 33 patients with PiB(-) SVaD, 17 patients with PiB(+) SVaD, and 64 normal controls. Seed-based analysis was used to assess functional connectivity in resting state fMRI. DMN was assessed by positive correlating areas with the posterior cingulated cortex (PCC). Relative to normal controls, DMN in PiB(+) AD showed decreased connectivity in bilateral PCC, anterior cingulated cortex (ACC), and medial temporal areas while increased connectivity was seen in right insular and cerebellar areas. In PiB(-) SVaD, there were no areas that showed decreased functional connectivity while increased connectivity was seen in bilateral prefrontal cortex when compared to normal controls. In PiB(+) SVaD more widespread areas showed decreased functional connectivity which included bilateral PCC, medial and lateral temporal, and ACC while increased connectivity was seen bilateral precuneus and dorsolateral frontal areas. In this study, PiB (-) SVaD had no disruption in DMN connectivity. Moreover PiB (+) SVaD had more widespread decreased and increased DMN than PiB (+) AD, suggesting small vessel disease and amyloid burdens might synergistically affect DMN.

Amnestic mild cognitive impairment (aMCI) represents a pre-dementia stage of Alzheimer's disease (AD). According to the severity of objective memory impairment, aMCI patients can be classified into subjects with milder degree of impairment and those with more severe impairment. Although previous studies showed that aMCI subjects with milder memory impairment have slower rates of AD progression than those with more severe memory impairment, there has been no study comparing regional cortical thickness according to this classification of aMCI. Cortical thickness across the entire brain and neuropsychological performance were measured in 271 patients with aMCI and 234 subjects with normal cognition (NC). According to the performances in delayed recall items of memory tests, aMCI patients were divided into early-stage aMCI (EMCI, N = 91) with milder degree of memory impairment (scores between -1.5 SD and -1.0 SD compared to age-, sex-, and education-matched norms) and late-stage MCI (LMCI, N = 180) with more severe memory impairment (lower than -1.5 SD). We performed ANCOVAs to compare neuropsychological performances and vertex-wise cortical thinning in EMCI, LMCI, and NC. Compared to NC subjects, EMCI patients showed cortical thinning in the left medial temporal lobe, and LMCI patients showed cortical thinning in bilateral medial temporal lobes, bilateral medial and lateral parietal cortices, bilateral dorsolateral prefrontal cortices, right posterior cingulate cortex, and bilateral anterior temporal cortices. When the two aMCI groups were directly compared, LMCI patients showed more cortical thinning in the right medial temporal lobe, right posterior cingulate cortex, right lateral parietal cortex, and right dorsolateral prefrontal cortex. Both EMCI and LMCI patients showed lower performances in all neuropsychological tests compared to NC. When directly compared with EMCI, LMCI subjects had poorer performance in all memory tests and COWAT supermarket test, while having comparable scores in other tests.

Hippocampal atrophy (HA) is a key characteristic in patients with Alzheimer's disease (AD). However, it has been documented in other dementias including vascular dementia (VaD). Many studies hypothesized that HA in VaD might come from either combined AD pathology or some accumulating burden of ischemia. Most previous studies which described HA in VaD, however, did not distinguish mixed AD with small vessel disease from pure VaD. Therefore, the purposes of the current study were to explore whether the HA exists or not in patients with pure subcortical VaD (SVaD) defined by the absence of amyloid deposition in 11 C-Pittsburgh compound B (PIB) positron emission tomography (PET), and to compare hippocampal shape between PIB (-) ,PIB (+) SVaD and AD patients. We studied 41 patients with 27 with PIB (-) SVaD and 14 with PIB (+) SVaD, 35 with AD and 22 with healthy cognitively normal subjects (NCI). Brain amyloid deposition was measured by PIB-PET in patients with SVaD and AD. Hippocampal surfaces, represented by 3D triangular meshes, were used for analyzing the shape difference and volume changes. Volumetric analysis of hippocampus revealed the mean hippocampal volume was significantly reduced in PIB (-) SVaD and PIB (+) group compared to NCI. There was no statistical difference of hippocampal volume between PIB (-) and PIB (+) SVaD after adjusting age and intracerebral volume. The shape analysis demonstrated that hippocampal shape differed between PIB (-) and PIB (+) SVaD patients, especially in the CA 1 region. Compared to AD, there was no statistical shape difference of hippocampus in PIB (+) SVaD patients.