Publications
282 results found
Alexopoulos P, Kriett L, Haller B, et al., 2014, Limited agreement between biomarkers of neuronal injury at different stages of Alzheimer's disease, ALZHEIMERS & DEMENTIA, Vol: 10, Pages: 684-689, ISSN: 1552-5260
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- Citations: 46
Perani D, Della Rosa PA, Cerami C, et al., 2014, Validation of an optimized SPM procedure for FDG-PET in dementia diagnosis in a clinical setting, NEUROIMAGE-CLINICAL, Vol: 6, Pages: 445-454, ISSN: 2213-1582
Diagnostic accuracy in FDG-PET imaging highly depends on the operating procedures. In this clinical study on dementia, we compared the diagnostic accuracy at a single-subject level of a) Clinical Scenarios, b) Standard FDG Images and c) Statistical Parametrical (SPM) Maps generated via a new optimized SPM procedure. We evaluated the added value of FDG-PET, either Standard FDG Images or SPM Maps, to Clinical Scenarios. In 88 patients with neurodegenerative diseases (Alzheimer's Disease—AD, Frontotemporal Lobar Degeneration—FTLD, Dementia with Lewy bodies—DLB and Mild Cognitive Impairment—MCI), 9 neuroimaging experts made a forced diagnostic decision on the basis of the evaluation of the three types of information. There was also the possibility of a decision of normality on the FDG-PET images. The clinical diagnosis confirmed at a long-term follow-up was used as the gold standard. SPM Maps showed higher sensitivity and specificity (96% and 84%), and better diagnostic positive (6.8) and negative (0.05) likelihood ratios compared to Clinical Scenarios and Standard FDG Images. SPM Maps increased diagnostic accuracy for differential diagnosis (AD vs. FTD; beta 1.414, p = 0.019). The AUC of the ROC curve was 0.67 for SPM Maps, 0.57 for Clinical Scenarios and 0.50 for Standard FDG Images. In the MCI group, SPM Maps showed the highest predictive prognostic value (mean LOC = 2.46), by identifying either normal brain metabolism (exclusionary role) or hypometabolic patterns typical of different neurodegenerative conditions.
Perneczky R, Alexopoulos P, 2014, Cerebrospinal fluid BACE1 activity and markers of amyloid precursor protein metabolism and axonal degeneration in Alzheimer's disease, ALZHEIMERS & DEMENTIA, Vol: 10, Pages: S425-+, ISSN: 1552-5260
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- Citations: 31
Morbelli S, Brugnolo A, Bossert I, et al., 2014, Visual versus semi-quantitative analysis of 18F-FDG PET in amnestic mild cognitive impairment (MCI) in the era of early Alzheimer's diagnosis. A project of the European Alzheimer's Disease Consortium (EADC), Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), Publisher: SPRINGER, Pages: S617-S618, ISSN: 1619-7070
van der Zee J, Van Langenhove T, Kovacs GG, et al., 2014, Rare mutations in SQSTM1 modify susceptibility to frontotemporal lobar degeneration, ACTA NEUROPATHOLOGICA, Vol: 128, Pages: 397-410, ISSN: 0001-6322
Mutations in the gene coding for Sequestosome 1 (SQSTM1) have been genetically associated with amyotrophic lateral sclerosis (ALS) and Paget disease of bone. In the present study, we analyzed the SQSTM1 coding sequence for mutations in an extended cohort of 1,808 patients with frontotemporal lobar degeneration (FTLD), ascertained within the European Early-Onset Dementia consortium. As control dataset, we sequenced 1,625 European control individuals and analyzed whole-exome sequence data of 2,274 German individuals (total n = 3,899). Association of rare SQSTM1 mutations was calculated in a meta-analysis of 4,332 FTLD and 10,240 control alleles. We identified 25 coding variants in FTLD patients of which 10 have not been described. Fifteen mutations were absent in the control individuals (carrier frequency <0.00026) whilst the others were rare in both patients and control individuals. When pooling all variants with a minor allele frequency <0.01, an overall frequency of 3.2 % was calculated in patients. Rare variant association analysis between patients and controls showed no difference over the whole protein, but suggested that rare mutations clustering in the UBA domain of SQSTM1 may influence disease susceptibility by doubling the risk for FTLD (RR = 2.18 [95 % CI 1.24–3.85]; corrected p value = 0.042). Detailed histopathology demonstrated that mutations in SQSTM1 associate with widespread neuronal and glial phospho-TDP-43 pathology. With this study, we provide further evidence for a putative role of rare mutations in SQSTM1 in the genetic etiology of FTLD and showed that, comparable to other FTLD/ALS genes, SQSTM1 mutations are associated with TDP-43 pathology.
Ferrari R, Hernandez DG, Nalls MA, et al., 2014, Frontotemporal dementia and its subtypes: a genome-wide association study, LANCET NEUROLOGY, Vol: 13, Pages: 686-699, ISSN: 1474-4422
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- Citations: 232
Yakushev I, Kriett L, Perneczky R, et al., 2014, Limited agreement between biomarkers of neuronal injury at different stages of Alzheimer's disease, Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging (SNMMI), Publisher: SOC NUCLEAR MEDICINE INC, ISSN: 0161-5505
Titov D, Li J, Foerster S, et al., 2014, Covariance-based differentiation of neurodegenerative dementias with 18F-FDG-PET, Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging (SNMMI), Publisher: SOC NUCLEAR MEDICINE INC, ISSN: 0161-5505
Titov D, Li J, Foerster S, et al., 2014, Covariance-based differentiation of neurodegenerative dementias with 18F-FDG-PET, Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging (SNMMI), Publisher: SOC NUCLEAR MEDICINE INC, ISSN: 0161-5505
Yakushev I, Kriett L, Perneczky R, et al., 2014, Limited agreement between biomarkers of neuronal injury at different stages of Alzheimer's disease, Annual Meeting of the Society-of-Nuclear-Medicine-and-Molecular-Imaging (SNMMI), Publisher: SOC NUCLEAR MEDICINE INC, ISSN: 0161-5505
Perneczky R, Alexopoulos P, Kurz A, 2014, Soluble amyloid precursor proteins and secretases as Alzheimer's disease biomarkers, TRENDS IN MOLECULAR MEDICINE, Vol: 20, Pages: 8-15, ISSN: 1471-4914
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- Citations: 34
Ferrari R, Hernandez DG, Nalls MA, et al., 2014, Genetic analysis suggests lysosomal and immune system involvement in frontotemporal dementia, Publisher: IOS PRESS, Pages: S25-S26, ISSN: 1387-2877
Grimmer T, Goldhardt O, Guo L-H, et al., 2014, LRP-1 polymorphism is associated with global and regional amyloid load in Alzheimer's disease in humans in-vivo, NEUROIMAGE-CLINICAL, Vol: 4, Pages: 411-416, ISSN: 2213-1582
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- Citations: 13
Picco A, Bossert I, Buschiazzo A, et al., 2014, Performance of [18F]FDG-PET in 142 MCI pazients with at least 2 years clinical follow up: a multicentric study of the European Alzheimer Disease Consortium (EADC), JOURNAL OF ALZHEIMERS DISEASE, Vol: 41, Pages: S39-S40, ISSN: 1387-2877
Perneczky R, Alexopoulos P, 2014, NOVEL UPSTREAM MARKERS OF AMYLOID PRECURSOR PROTEIN PROCESSING IN THE DIAGNOSIS AND PROGNOSIS OF ALZHEIMER'S DISEASE, EUROPEAN PSYCHIATRY, Vol: 29, ISSN: 0924-9338
Zech M, Nuebling G, Castrop F, et al., 2013, Niemann-Pick C Disease Gene Mutations and Age-Related Neurodegenerative Disorders, PLOS ONE, Vol: 8, ISSN: 1932-6203
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- Citations: 40
Morbelli S, Perneczky R, Drzezga A, et al., 2013, Metabolic Networks Underlying Cognitive Reserve in Prodromal Alzheimer Disease: A European Alzheimer Disease Consortium Project, JOURNAL OF NUCLEAR MEDICINE, Vol: 54, Pages: 894-902, ISSN: 0161-5505
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- Citations: 91
Diehl-Schmid J, Perneczky R, Koch J, et al., 2013, Guilty by Suspicion? Criminal Behavior in Frontotemporal Lobar Degeneration, COGNITIVE AND BEHAVIORAL NEUROLOGY, Vol: 26, Pages: 73-77, ISSN: 1543-3633
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- Citations: 38
Grimmer T, Wutz C, Drzezga A, et al., 2013, The usefulness of amyloid imaging in predicting the clinical outcome after two years in subjects with mild cognitive impairment, Curr Alzheimer Res, Vol: 10, Pages: 82-85, ISSN: 1875-5828
BACKGROUND: Mild cognitive impairment (MCI) is a syndrome heterogeneous with regards to etiology and prognosis. Amyloid imaging enables to visualize a hallmark pathology of Alzheimer's disease (AD). Therefore we aimed to assess the usefulness of [(11)C]PiB PET for predicting clinical outcome of MCI patients after an interval of 2 years. METHODS: In 28 MCI participants with a global CDR rating at baseline of 0.5 a baseline examination including clinical assessments and [(11)C]PiB PET imaging and a clinical follow-up examination after a planned interval of 24 months were performed. Predictive values and accuracy of amyloid-positive and negative scans for conversion to dementia of any type and to dementia due to AD were calculated and compared to neuropsychological tests and ApoE genotyping. RESULTS: Of 17 MCI patients who were amyloid-positive at baseline converted 9 to dementia all of the AD type. 3 of the 11 amyloid-negative MCI subjects converted to dementia but none to dementia due to AD. PPV, NPV and accuracy (to dementia: 0.53, 0.73 and 0.61; to AD: 0.53, 1.00 and 0.70) was comparable to neuropsychological tests and superior to ApoE genotyping. CONCLUSION: All MCI subjects who converted to dementia due to AD were amyloid-positive. However, only 50% of these MCI due to AD, intermediate likelihood, patients developed manifest dementia due to AD after 24 months limiting the usefulness of [(11)C]PiB PET for individual prediction of clinical outcome.
Guo LH, Alexopoulos P, Perneczky R, 2013, Heart-type fatty acid binding protein and vascular endothelial growth factor: cerebrospinal fluid biomarker candidates for Alzheimer's disease, Eur Arch Psychiatry Clin Neurosci, ISSN: 1433-8491
The main objective of the study was to validate the findings of previous cerebrospinal fluid (CSF) proteomic studies for the differentiation between Alzheimer's disease (AD) dementia and physiological ageing. The most consistently significant proteins in the separation between AD dementia versus normal controls using CSF proteomics were identified in the literature. The classification performance of the four pre-selected proteins was explored in 92 controls, 149 patients with mild cognitive impairment (MCI), and 69 patients with AD dementia. Heart-type fatty acid binding protein (hFABP) and vascular endothelial growth factor (VEGF) CSF concentrations distinguished between healthy controls and patients with AD dementia with a sensitivity and specificity of 57 and 35 %, and 76 and 84 %, respectively. The optimal classification was achieved by a combination of the two additional CSF biomarker candidates in conjunction with the three established markers Amyloid-beta (Abeta)1-42, total-Tau (tTau), and phosphorylated-Tau (pTau)181, which resulted in a sensitivity of 83 % and a specificity of 86 %. hFABP also predicted the progression from MCI to AD dementia. The present study provides evidence in support of hFABP and VEGF in CSF as AD biomarker candidates to be used in combination with the established markers Abeta1-42, tTau, and pTau181.
Morbelli S, Perneczky R, Drzezga A, et al., 2013, Metabolic Networks Underlying Cognitive Reserve in Prodromal Alzheimer Disease: A European Alzheimer Disease Consortium Project, J Nucl Med, ISSN: 1535-5667
This project aimed to investigate the metabolic basis for resilience to neurodegeneration (cognitive reserve) in highly educated patients with prodromal Alzheimer disease (AD). METHODS: Sixty-four patients with amnestic mild cognitive impairment who later converted to AD dementia during follow-up, and 90 controls, underwent brain 18F-FDG PET. Both groups were divided into a poorly educated subgroup (42 controls and 36 prodromal AD patients) and a highly educated subgroup (48 controls and 28 prodromal AD patients). Brain metabolism was first compared between education-matched groups of patients and controls. Then, metabolism was compared between highly and poorly educated prodromal AD patients in both directions to identify regions of high education-related metabolic depression and compensation. The clusters of significant depression and compensation were further used as volumetric regions of interest (ROIs) in a brain interregional correlation analysis in each prodromal AD subgroup to explore metabolic connectivity. All analyses were performed by means of SPM8 (P < 0.001 uncorrected at peak level, P < 0.05 false discovery rate-corrected at cluster level; age, sex, Mini-Mental State Examination score, and center as nuisance). RESULTS: Highly educated prodromal AD patients showed more severe hypometabolism than poorly educated prodromal AD patients in the left inferior and middle temporal gyri and the left middle occipital gyrus (ROI depression). Conversely, they showed relative hypermetabolism in the right inferior, middle, and superior frontal gyri (ROI compensation). The sites of compensation, mainly corresponding to the right dorsolateral prefrontal cortex (DLFC), showed wide metabolic correlations with several cortical areas in both hemispheres (frontotemporal cortex, parahippocampal gyrus, and precuneus) in highly educated prodromal AD patients but not in poorly educated prodromal AD patients. To provide evidence on whether these metabolic correlations rep
van der Zee J, Gijselinck I, Dillen L, et al., 2013, A pan-European study of the C9orf72 repeat associated with FTLD: geographic prevalence, genomic instability, and intermediate repeats, Hum Mutat, Vol: 34, Pages: 363-373, ISSN: 1098-1004
We assessed the geographical distribution of C9orf72 G(4) C(2) expansions in a pan-European frontotemporal lobar degeneration (FTLD) cohort (n = 1,205), ascertained by the European Early-Onset Dementia (EOD) consortium. Next, we performed a meta-analysis of our data and that of other European studies, together 2,668 patients from 15 Western European countries. The frequency of the C9orf72 expansions in Western Europe was 9.98% in overall FTLD, with 18.52% in familial, and 6.26% in sporadic FTLD patients. Outliers were Finland and Sweden with overall frequencies of respectively 29.33% and 20.73%, but also Spain with 25.49%. In contrast, prevalence in Germany was limited to 4.82%. In addition, we studied the role of intermediate repeats (7-24 repeat units), which are strongly correlated with the risk haplotype, on disease and C9orf72 expression. In vitro reporter gene expression studies demonstrated significantly decreased transcriptional activity of C9orf72 with increasing number of normal repeat units, indicating that intermediate repeats might act as predisposing alleles and in favor of the loss-of-function disease mechanism. Further, we observed a significantly increased frequency of short indels in the GC-rich low complexity sequence adjacent to the G(4) C(2) repeat in C9orf72 expansion carriers (P < 0.001) with the most common indel creating one long contiguous imperfect G(4) C(2) repeat, which is likely more prone to replication slippage and pathological expansion.
Dukart J, Perneczky R, Forster S, et al., 2013, Reference cluster normalization improves detection of frontotemporal lobar degeneration by means of FDG-PET, PLoS One, Vol: 8, ISSN: 1932-6203
Positron emission tomography with [18F] fluorodeoxyglucose (FDG-PET) plays a well-established role in assisting early detection of frontotemporal lobar degeneration (FTLD). Here, we examined the impact of intensity normalization to different reference areas on accuracy of FDG-PET to discriminate between patients with mild FTLD and healthy elderly subjects. FDG-PET was conducted at two centers using different acquisition protocols: 41 FTLD patients and 42 controls were studied at center 1, 11 FTLD patients and 13 controls were studied at center 2. All PET images were intensity normalized to the cerebellum, primary sensorimotor cortex (SMC), cerebral global mean (CGM), and a reference cluster with most preserved FDG uptake in the aforementioned patients group of center 1. Metabolic deficits in the patient group at center 1 appeared 1.5, 3.6, and 4.6 times greater in spatial extent, when tracer uptake was normalized to the reference cluster rather than to the cerebellum, SMC, and CGM, respectively. Logistic regression analyses based on normalized values from FTLD-typical regions showed that at center 1, cerebellar, SMC, CGM, and cluster normalizations differentiated patients from controls with accuracies of 86%, 76%, 75% and 90%, respectively. A similar order of effects was found at center 2. Cluster normalization leads to a significant increase of statistical power in detecting early FTLD-associated metabolic deficits. The established FTLD-specific cluster can be used to improve detection of FTLD on a single case basis at independent centers - a decisive step towards early diagnosis and prediction of FTLD syndromes enabling specific therapies in the future.
Alexopoulos P, Guo LH, Jiang M, et al., 2013, Amyloid Cascade and Tau Pathology Cerebrospinal Fluid Markers in Mild Cognitive Impairment with regards to Alzheimer's Disease Cerebral Metabolic Signature, J Alzheimers Dis, ISSN: 1875-8908
Background: Biomarker relationships in early stages of Alzheimer's disease (AD) are elusive. Cerebrospinal fluid (CSF) levels of amyloid-beta 1-42 (Abeta42) and total tau (tTau) as well as 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) contribute to help unravel AD pathology. Furthermore, peptides related to amyloid-beta protein precursor (AbetaPP) processing [e.g., soluble AbetaPPalpha and beta (sAbetaPPalpha and sAbetaPPbeta, respectively); sortilin-related receptor with A-type repeats (SORL1, also called LR11 or SORLA)] are factors crucially implicated in the formation of pathological hallmarks of AD. Objective: To unveil differences in CSF concentrations of Abeta42, sAbetaPPalpha, sAbetaPPbeta, tTau, and SORL1 between patients with mild cognitive impairment (MCI) who were categorized according to expert interpretation of FDG scans. Methods: PET results were classified as suggesting high likelihood for AD (MCI-AD high), intermediate likelihood for AD (MCI-AD intermediate), or little likelihood for AD (MCI-AD unlikely). An AD dementia group was also included. Differences between the groups were tested by Kruskal- Wallis test, Mann-Whitney test, or chi2. Provided statistically significant differences were detected, multiple linear regression models were employed. Results: Abeta42 levels in patients with MCI-AD high (n = 15) were lower compared to MCI-AD intermediate (n = 18) and MCI-AD unlikely patients (n = 25) (p = 0.002), while they did not differ from patients with AD dementia (n = 17). The regression model revealed a significant impact of the metabolic pattern on Abeta42 concentrations. SORL1, tTau, sAbetaPPalpha, and sAbetaPPbeta concentrations did not differ between the groups. Conclusion: These findings point to linkages between plaque pathology and glucose cerebral hypometabolism.
Perneczky R, Guo LH, Kagerbauer SM, et al., 2013, Soluble amyloid precursor protein beta as blood-based biomarker of Alzheimer's disease, Transl Psychiatry, Vol: 3, ISSN: 2158-3188
The aim of this study was to explore concentrations differences of soluble amyloid precursor protein (sAPP) alpha and beta in blood plasma in patients with probable Alzheimer's disease (AD) and cognitively healthy age-matched control subjects, as well as patients with behavioural variant frontotemporal dementia (bvFTD). Concentrations of sAPPalpha and beta were measured using enzyme-linked immunosorbent assay technology in 80 patients with probable AD, 37 age-matched control subjects and 14 patients with bvFTD. Concentration differences were explored using parametric tests. Significantly decreased plasma concentrations in the AD group compared with both the control group and the bvFTD group were detected for sAPPbeta (P = 0.03 for both group comparisons), but not for sAPPalpha. The study provides a further piece of evidence in support of sAPPbeta as a promising new biomarker of AD, which may potentially improve the diagnostic accuracy of existing markers and also enable a less invasive diagnostic workup. Further research is required to establish normal ranges and to replicate the results in independent cohorts including larger numbers of participants covering a wider spectrum of cognitive impairment.
Guo LH, Alexopoulos P, Wagenpfeil S, et al., 2013, Plasma Proteomics for the Identification of Alzheimer Disease, Alzheimer Dis Assoc Disord, ISSN: 1546-4156
Less-invasive biomarkers for early Alzheimer disease (AD) are urgently needed. The present study aimed to establish a panel of plasma proteins that accurately distinguishes early AD from physiological aging and to compare the findings with previous reports. Fifty-eight healthy controls (CON) and 109 patients with AD dementia were randomly split into a training (40%) and a test (60%) sample. Significant proteins to differentiate between the CON and AD dementia groups were identified in a comprehensive panel of 107 plasma analytes in the training sample; the accuracy in differentiating these 2 groups was explored in the test sample. A set of 5 plasma proteins was identified, which differentiated between the CON group and the AD dementia group with a sensitivity of 89.36% and a specificity of 79.17%. A biological pathway analysis showed that 4 of 5 proteins belonged to a common network with amyloid precursor protein and tau. Apolipoprotein E was the only protein that was both significant in the present report and in a previous proteomic study. The study provides a piece of evidence in support of the feasibility of a blood-based biomarker approach in AD diagnostics; however, further research is required because of issues with replicability.
Dukart J, Perneczky R, Foerster S, et al., 2012, Reference cluster normalization improves detection of frontotemporal lobar degeneration, Publisher: SOC NUCLEAR MEDICINE INC, ISSN: 0161-5505
Grimmer T, Alexopoulos P, Tsolakidou A, et al., 2012, Cerebrospinal fluid BACE1 activity and brain amyloid load in Alzheimer's disease, The Scientific World Journal, Vol: 2012, ISSN: 1537-744X
The secretase BACE1 is fundamentally involved in the development of cerebral amyloid pathology in Alzheimer's disease (AD). It has not been studied so far to what extent BACE1 activity in cerebrospinal fluid (CSF) mirrors in vivo amyloid load in AD. We explored associations between CSF BACE1 activity and fibrillar amyloid pathology as measured by carbon-11-labelled Pittsburgh Compound B positron emission tomography ([(1)(1)C]PIB PET). [(1)(1)C]PIB and CSF studies were performed in 31 patients with AD. Voxel-based linear regression analysis revealed significant associations between CSF BACE1 activity and [(1)(1)C]PIB tracer uptake in the bilateral parahippocampal region, the thalamus, and the pons. Our study provides evidence for a brain region-specific correlation between CSF BACE1 activity and in-vivo fibrillar amyloid pathology in AD. Associations were found in areas close to the brain ventricles, which may have important implications for the use of BACE1 in CSF as a marker for AD pathology and for antiamyloid treatment monitoring.
Alexopoulos P, Guo LH, Tsolakidou A, et al., 2012, Interrelations between CSF soluble AbetaPPbeta, amyloid-beta 1-42, SORL1, and tau levels in Alzheimer's disease, J Alzheimers Dis, Vol: 28, Pages: 543-552, ISSN: 1875-8908
Recently, light has been shed on possible interrelations between the two most important pathological hallmarks of Alzheimer's disease (AD): the amyloid cascade and axonal degeneration. In this study, we investigated associations between sbetaAPPbeta, a product of the cleavage of the amyloid-beta protein precursor (AbetaPP) by beta-secretase, amyloid-beta 1-42 (Abeta42), soluble SORL1 (also called LR11 or SORLA), a receptor that is involved in AbetaPP processing, and the marker of axonal degeneration tau in the cerebrospinal fluid (CSF) of 76 patients with mild cognitive impairment (MCI), 61 patients with AD, and 17 patients with frontotemporal dementia, which neuropathologically is not related to the amyloid pathology. In the AD group, significant associations between sAbetaPPbeta, tau (p < 0.001), and soluble SORL1 (p < 0.001) were detected according to linear regression models. In patients with MCI, sAbetaPPbeta correlated significantly with tau (p < 0.001) and soluble SORL1 (p = 0.003). In the FTD group, only SORL1 (p = 0.011) was associated with sAbetaPPbeta and not tau. Abeta42 was found to be significantly related to tau levels in CSF in the MCI group (p < 0.001) and they tended to be associated in the AD group (p = 0.05). Our results provide further evidence for a link between the two facets of AD pathology, which is likely to be mediated by the binding of Abeta oligomers to specifically targeted neurons, resulting in stimulating tau hyperphosphorylation and neurodegeneration.
Alexopoulos P, Sorg C, Forschler A, et al., 2012, Perfusion abnormalities in mild cognitive impairment and mild dementia in Alzheimer's disease measured by pulsed arterial spin labeling MRI, Eur Arch Psychiatry Clin Neurosci, Vol: 262, Pages: 69-77, ISSN: 1433-8491
Alzheimer's disease (AD) and mild cognitive impairment (MCI), the transitional clinical stage between cognition in normal aging and dementia, have been linked to abnormalities in brain perfusion. Pulsed arterial spin labeling (PASL) is a magnetic resonance imaging (MRI) technique for evaluating brain perfusion. The present study aimed to determine regional perfusion abnormalities in 19 patients with mild dementia in AD and 24 patients with MCI as compared to 24 cognitively healthy elderly controls using PASL. In line with nuclear imaging methods, lower perfusion in patients with MCI and AD was found mainly in the parietal lobe, but also in angular and middle temporal areas as well as in the left middle occipital lobe and precuneus. Our data imply that PASL may be a valuable instrument for investigating perfusion changes in the transition from normal aging to dementia and indicate that it might become an alternative to nuclear imaging techniques in AD diagnostics.
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