Alzheimer Disease: Frisoni GB

Frisoni GB, Whitwell JL. · No affiliation provided · Neurology. · Pubmed #18519869 No free full text.

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Frisoni GB, Padovani A, Wahlund LO. · No affiliation provided · Alzheimer Dis Assoc Disord. · Pubmed #15249846 No free full text.

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Frisoni GB. · No affiliation provided · J Neurol Neurosurg Psychiatry. · Pubmed #11384998 links to  free full text

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Frisoni GB. · No affiliation provided · J Neurol Neurosurg Psychiatry. · Pubmed #11032603 links to  free full text

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Galluzzi S, Frisoni GB. · Laboratory of Epidemiology, Neuroimaging and Telemedicine IRCCS San Giovanni di Dio - FBF, via Pilastroni 4, 25125 Brescia, Italy. · J Nutr Health Aging. · Pubmed #18165851 No free full text.

Abstract: The neuropathological and cognitive changes preceding Alzheimer's disease (AD) appear to begin decades before disease symptoms make the clinical diagnosis obvious. Clinical trials have begun to focus on preventive treatments aimed to slow cognitive decline in people with only subjective memory complaints. However, it is not clear how many years before clinical diagnosis of Alzheimer's disease is possible to recognize early signs of neurodegeneration. We report evidence from the literature showing feasibility to diagnose AD at the stage of mild cognitive impairment (MCI) and also a few years before the MCI stage with imaging markers. However, we showed that neuroimaging brain changes evidenced decades before MCI are not early signs of neurodegeneration but expression of genetic risk states for AD or markers of inter-individual variability of cognitive performance due to genetic or environmental factors.

Frisoni GB, Caroli A. · G.B. Frisoni, IRCCS Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy. · J Nutr Health Aging. · Pubmed #17653497 No free full text.

Abstract: A wide range of drugs is currently under development for treating Alzheimer's Disease (AD). Clinical trials traditionally use rating scales, such as neuropsychological tests and disability scales, as outcome measures. However, their intrinsic measurement variability, the slow disease progression, and the low effectiveness of the drugs developed so far have led to trial designs with hundreds of subjects per treatment arm. Furthermore, a key issue is to establish what effect are these compounds having on the biological progression of the disease, beyond delaying symptomatic progression. The development of imaging markers, either structural, functional, or amyloid, with proven sensitivity to disease progression has recently paved the way for their use as outcome measures in clinical trials. The use of imaging measures has the double advantage of decreasing the number of subjects per treatment arm whilst also providing a direct measure of the degree of disease modification induced by the "active" molecules. The reviewed techniques, except for the most recent amyloid imaging, are those applied to prospective studies investigating changes of imaging markers over time.

Frisoni GB, Filippi M. · Laboratory of Epidemiology NeuroImaging and TeleMedicine, IRCCS San Giovanni di Dio FBF, Brescia, Italy. · AJNR Am J Neuroradiol. · Pubmed #16286389 links to  free full text

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Frisoni GB. · Laboratory of Epidemiology & Neuroimaging, IRCCS San Giovanni di Dio-FBF, Brescia, Italy. · J Neurol. · Pubmed #11517995 No free full text.

Abstract: Views on drug therapy with acetylcholinesterase inhibitors of the cognitive symptoms of Alzheimer's disease are not uniform, varying from excitement at the possibility of significantly improving the personal and social burden of the disease to skeptical and nihilistic attitudes. Clinical practice from generous prescription to evidence-based guidelines and advising much stricter rules, mirror these attitudes. The epidemiological and clinical relevance of the issue requires understanding of the factors responsible for such discrepancies. Randomized clinical trials have only been able to address a few of the many variables that can affect the response to acetylcholinesterase inhibitors. The effect on behavioral symptoms, severe Alzheimer's dementia, and non-Alzheimer's forms of degenerative dementia need to be clarified as well as the modulating effect of frequently associated conditions such as cognitive changes due to physical diseases and cerebrovascular disease. The gap between evidence and clinical practice might be closed with appropriately designed observational studies rather than randomized clinical trials.

Galluzzi S, Cimaschi L, Ferrucci L, Frisoni GB. · Laboratory of Epidemiology and Neuroimaging, IRCCS San Giovanni di Dio, FBF, Brescia, Italy. · Aging (Milano). · Pubmed #11442301 No free full text.

Abstract: Clinical criteria to recognize subjects with cognitive impairment in the pre-dementia stage are becoming available. These are frail subjects, at risk of adverse outcomes, such as death, institutionalization, and functional and cognitive deterioration. Early identification of these subjects has a great importance in order to start rehabilitative or pharmacological interventions that could slow the progression of cognitive impairment, and the onset of disability. In this regard, cognitive screening tests might be helpful in different clinical settings (general practice, acute care, rehabilitation, and nursing home). We describe the most frequent clinical presentations of cognitive impairment in the pre-dementia stage, and review eleven screening tests to provide recommendations on which should be preferred in each setting.

Riello R, Frisoni GB. · Laboratorio di Epidemiologia e Neuroimaging, IRCCS San Giovanni di Dio, Fatebenefratelli, Brescia. · Recenti Prog Med. · Pubmed #11413888 No free full text.

Abstract: The application of music therapy to Alzheimer's patients is relatively recent. The studies available in literature show that music therapy has a positive effect either on mood or cognition. However, the generalization of data is difficult because these researches have lacked methodological design rigour. Based on the application of this rehabilitative technique in our Alzheimer Unit in Brescia and on the recent researches of music neuroanatomy, this work tries to identify which processes are involved in the therapeutic effect of music therapy. Despite the perceived effect on mood and socialisation abilities, cultural and methodological problems hinder to demonstrate the efficacy of music therapy. Information about neurophysiological and neurochemical correlates of music therapy are so poor that the use of this technique is often based on the assumption that the supposed positive effect of music is enough to justify its application. The methodological problem is related to the evaluation of outcomes. The fact that those studies which investigated the effects of music therapy were characterized by less specific indicators (cognition, behavior) and by less standardized instruments made difficult to generalize and quantify the results. The aim of the study is to organize the present knowledge with a systematic approach so that further researches lead to base the application of music therapy on evidence instead of on singular clinical finding.

Lehtovirta M, Laakso MP, Frisoni GB, Soininen H. · Department of Neurology, Kuopio University Hospital, P.O. Box 1777, 70211, Kuopio, Finland. · Neurobiol Aging. · Pubmed #10867214 No free full text.

Abstract: The epsilon 4 allele of apolipoprotein E is a risk factor for Alzheimer's disease, but also a modulator of its clinical picture. In this paper, recent research in neuroimaging of aging and Alzheimer's disease in relation to apolipoprotein E is reviewed, emphasizing the advances but also the controversies. Further, the possible clinicopathological implications of these findings are discussed.

Prestia A, Rossi R, Geroldi C, Galluzzi S, Ettori M, Alaimo G, Frisoni GB. · Associazione Fatebenefratelli per la Ricerca, Rome, Italy. · Exp Aging Res. · Pubmed #16982570 No free full text.

Abstract: The aim of the present study was to validate a short, ecological test of episodic memory for the screening of Alzheimer's disease (AD). The validation was performed by computing intrarater reliability, homogeneity, internal coherence, convergent, discriminant and known group validities in the performance of normal subjects (N = 65), mild cognitive impairment (MCI) patients (N = 114), and AD (N = 44) and non-AD demented (N = 39) patients. Intrarater reliability was 0.88, homogeneity ranged from 0.81 to 0.97, and internal coherence was 0.87. With respect to convergent and discriminant validities, the test loaded strongly on memory factor (value = 0.64) and weakly on other nonmemory factors. The known group validity showed a specificity between 87% and 91% and a sensitivity between 92% and 100% in correctly identifying AD in age classes ranging from 50 to 65 and 66 to 80 years. The test is a valid instrument for the screening of AD.

Geroldi C, Rossi R, Calvagna C, Testa C, Bresciani L, Binetti G, Zanetti O, Frisoni GB. · Laboratory of Epidemiology, Neuroimaging and Telemedicine, IRCCS San Giovanni di Dio FBF-The National Center for Research and Care of Alzheimer's Disease, via Pilastroni 4, 25125 Brescia, Italy. · J Neurol Neurosurg Psychiatry. · Pubmed #16891386 No free full text.

Abstract: BACKGROUND: The diagnosis of mild cognitive impairment (MCI) is clinically unhelpful, as many patients with MCI develop dementia but many do not. OBJECTIVE: To identify clinical instruments easily applicable in the clinical routine that might be useful to predict progression to dementia in patients with MCI assessed in the outpatient facility of a memory clinic. PARTICIPANTS AND METHODS: 52 dementia-free patients (mean (standard deviation) age 70 (6) years; 56% women) with MCI, and 65 healthy controls (age 69 (6) years; 54% women) underwent brain magnetic resonance scan with standardised visual assessment of medial temporal atrophy (MTA) and subcortical cerebrovascular lesions (SVLs). Follow-up assessment occurred 15.4 (SD 3.4) months after baseline to detect incident dementia and improvement, defined as normal neuropsychological performance on follow-up. RESULTS: Patients were classified into three groups according to the presence of memory disturbance only (MCI Mem), other neuropsychological deficits (MCI Oth) or both (MCI Mem+). MCI Mem and Mem+ showed MTA more frequently (31% and 47% v 5% and 14% of controls and MCI Oth, p<0.001). 11 patients developed dementia (annual rate 16.5%) and 7 improved on follow-up. The only independent predictor of progression was MTA (odds ratio (OR) 7.1, 95% confidence interval (CI) 1.4 to 35.0), whereas predictors of improvement were the absence of memory impairment (OR 18.5, 95% CI 2.0 to 171.3) and normal MRI scan (OR 10.0, 95% CI 1.7 to 60.2). CONCLUSION: Neuropsychological patterns identify groups of patients with MCI showing specific clinical features and risk of progression to dementia. MTA clinically rated with a visual scale is the most relevant predictor of progression and improvement.

Geroldi C, Akkawi NM, Galluzzi S, Ubezio M, Binetti G, Zanetti O, Trabucchi M, Frisoni GB. · Laboratory of Epidemiology and Neuroimaging, IRCCS San Giovanni di Dio, FBF, via Pilastroni 4, 25125 Brescia, Italy. · J Neurol Neurosurg Psychiatry. · Pubmed #10896691 links to  free full text

Abstract: OBJECTIVE: To test the hypothesis that delusions are associated with asymmetric involvement of the temporal lobe regions in Alzheimer's disease. METHODS: Temporal lobe atrophy was assessed with a linear measure of width of the temporal horn (WTH) taken from CT films. Temporal asymmetry was computed as the right/left (R/L) ratio of the WTH in 22 non-delusional and 19 delusional patients with Alzheimer's disease. Delusional patients had paranoid delusions (of theft, jealousy, persecution). None of the patients had misidentifications or other delusions of non-paranoid content. RESULTS: The R/L ratio indicated symmetric temporal horn size in the non-delusional (mean 1. 05 (SD 0.20), and right greater than left temporal horn in the delusional patients (mean 1.30, (SD 0.46); t=2.27, df=39, p=0.03). When patients were stratified into three groups according to the R/L ratio, 47% of the delusional (9/19) and 14% of the non-delusional patients (3/21; chi(2)=5.6, df=1, p=0.02) showed right markedly greater than left WTH. CONCLUSIONS: Predominantly right involvement of the medial temporal lobe might be a determinant of paranoid delusions in the mild stages of Alzheimer's disease.

Laakso MP, Frisoni GB, Könönen M, Mikkonen M, Beltramello A, Geroldi C, Bianchetti A, Trabucchi M, Soininen H, Aronen HJ. · Department of Neurology, Kuopio University Hospital, Finland. · Biol Psychiatry. · Pubmed #10862805 No free full text.

Abstract: BACKGROUND: Magnetic resonance imaging (MRI) of hippocampal atrophy is a sensitive but not specific method to support the clinical diagnosis of early Alzheimer's disease (AD). We recently described our findings that atrophy of the entorhinal cortex (ERC) in frontotemporal dementia (FTD) is equal to that found in AD but that hippocampal atrophy in FTD is less than that found in AD. The MRI volumes of these structures provide a topographic representation of the region of interest. We hypothesized that two different dementias with distinct histopathologic and clinical features might, in addition to quantitative patterns, display topographically different patterns of atrophy. METHODS: We adopted a morphometric approach to monitor the pattern of atrophy of the hippocampus and the ERC by computing two-dimensional profiles from MRI volumes of the structures in control subjects and patients with FTD and AD. RESULTS: Compared with control subjects, atrophy of the hippocampus in patients with AD was diffuse. In patients with FTD, atrophy of the hippocampus was localized predominantly in the anterior hippocampus, suggesting a different pattern of hippocampal atrophy in FTD compared with AD. The amount and pattern of atrophy of the entorhinal cortex was virtually equal in both demented groups. CONCLUSIONS: This study provides novel data on the nature of medial temporal lobe atrophy in FTD. Morphometric MRI may be a useful technique for characterizing different patterns of atrophy in primary degenerative dementias in vivo.

Frisoni GB, Bianchetti A, Pignatti F, Gozzetti A, Trabucchi M. · No affiliation provided · Am J Psychiatry. · Pubmed #10588430 links to  free full text

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Frisoni GB, Rozzini L, Gozzetti A, Binetti G, Zanetti O, Bianchetti A, Trabucchi M, Cummings JL. · Alzheimer's Unit, IRCCS S. Giovanni di Dio, 'Fatebenefratelli', Geriatric Research Group, Brescia, Italy. · Dement Geriatr Cogn Disord. · Pubmed #10026387 No free full text.

Abstract: INTRODUCTION: Behavioral disturbances in patients with Alzheimer's disease (AD) are ill-defined conditions. We hypothesize that the many behavioral disturbances hitherto described and studied might be grouped into few syndromes with separate determinants and correlates. PATIENTS AND METHODS: 162 consecutive patients with probable AD admitted to a dementia unit were assessed by the UCLA Neuropsychiatric Inventory (NPI). RESULTS: Factor analysis was carried out on NPI subscales, leading to three syndromes: 'mood', 'psychotic' and 'frontal'. Patients with the 'psychotic' syndrome were older, had older age at dementia onset, had poorer cognition, were more often males, and had faster rate of dementia progression. Patients with the 'frontal' syndrome had higher education, longer disease duration, and slower rate of progression. DISCUSSION: Some combinations of behavioral disturbances occur more frequently together and might represent separate behavioral syndromes. Different clinical correlates of the syndromes suggest separate etiologies.

Porteri C, Andreatta C, Anglani L, Pucci E, Frisoni GB. · Bioethics Unit, IRCCS, Centro San Giovanni di Dio Fatebenefratelli, Via Pilastroni 4, 25125 Brescia, Italy. · Aging Clin Exp Res. · Pubmed #19448388 No free full text.

Abstract: BACKGROUND: Because of the growing value attributed to informed consent, competence assessment has become an important task for physicians and researchers, particularly when treatment and research involve persons who may be cognitively impaired, such as those with Alzheimer's dementia. METHODS: We developed and validated a 12-item questionnaire to assess the understanding of information about clinical trials by research subjects (score 0 to 24). The 12 questions were selected from a larger pool of 16 through internal consistency validity testing. We used the instrument in a pilot study involving 42 patients with mild to moderate Alzheimer's disease who had been asked to take part in two randomized clinical trials, and 21 caregivers. RESULTS: Patients with Alzheimer's disease had poor understanding (mean global score on questionnaire: 6.1+/-3.5). Unlike patients, caregivers understand the key elements of the clinical trials (questionnaire mean global score: 21.5+/-2.3; p for difference with patients <0.0001). In the group of patients, the score on the questionnaire correlated weakly with the Mini Mental State Exam (r=0.351; p=0.023), but more strongly with years of education in the group of caregivers (r=0.548; p=0.010) and age (r=-0.540; p=0.011). CONCLUSIONS: Patients with Alzheimer's disease of mild to moderate severity show poor understanding of the design, risks and benefits of clinical trials. Enrolment of these patients in clinical trials must be accompanied by adequate measures for patient protection.

Frisoni GB, Lorenzi M, Caroli A, Kemppainen N, Någren K, Rinne JO. · Laboratory of Epidemiology and Neuroimaging, IRCCS San Giovanni di Dio-FBF, via Pilastroni 4, I-25123 Brescia, Italy. · Neurology. · Pubmed #19398705 No free full text.

Abstract: OBJECTIVE: To study the relationship between gray matter atrophy and amyloid deposition in Alzheimer disease (AD). METHODS: Volumetric magnetic resonance (MR) and [11C]-PIB PET were acquired from 23 patients with AD and 17 healthy older persons. Standardized [11C]-PIB uptake values were coregistered to MR scans in a standard space. Decreased density of and increased [11C]-PIB uptake in the gray matter of patients with AD vs controls were assessed with both voxel-based (p < 0.05 corrected) and region-of-interest (ROI) analyses. The relationship between decreased density of and increased [11C]-PIB uptake in the gray matter was investigated with voxel-based Pearson r maps (thresholded at p < 0.05) and ROI linear regression plots. RESULTS: Atrophy mapped to the hippocampus and increased [11C]-PIB uptake to large frontal, parietal, and posterior cingulate cortical areas. ROI analysis showed the largest effect size for atrophy in the hippocampus (2.01) and amygdala (1.27) and the highest effect size for [11C]-PIB uptake in frontal (2.66), posterior cingulate/retrosplenial (2.43), insular (2.41), and temporal (2.23) regions. In the hippocampus, [11C]-PIB uptake was significantly increased, but effect size was milder (1.72). Significant correlations between atrophy and increased [11C]-PIB uptake were found in the hippocampal (r = -0.54) and amygdalar ROIs (r = -0.40) but not in the frontal, temporal, posterior cingulate/retrosplenial, insular, and caudate ROIs (r between 0.04 and 0.25). CONCLUSION: The medial temporal lobe might be highly susceptible to amyloid toxicity, whereas neocortical areas might be more resilient.

Filippini N, Zarei M, Beckmann CF, Galluzzi S, Borsci G, Testa C, Bonetti M, Beltramello A, Ghidoni R, Benussi L, Binetti G, Frisoni GB. · LENITEM, Laboratory of Epidemiology, Neuroimaging, & Telemedicine- IRCCS S. Giovanni di Dio-FBF, Brescia, Italy. · J Magn Reson Imaging. · Pubmed #19388128 No free full text.

Abstract: PURPOSE: To investigate the possible effect of the APOE epsilon4 allele on age-related regional volume loss within the corpus callosum (CC) in healthy epsilon4 allele carriers compared with noncarriers. MATERIALS AND METHODS: A total of 211 subjects, ages 27 to 83 years, 51 epsilon4 carriers and 160 noncarriers underwent T1-weighted MRI scan. All subjects had normal MRI scan and performed within normal range on a neuropsychological battery of tests. CC was segmented into seven functionally relevant regions using a previously published probabilistic map of the CC connectivity. We measured the volumes of the CC and its subregions. We used a regression model (with volumes as dependent and age as independent variables) and compared the slopes between carriers and noncarriers using an analysis of covariance model. We also carried out voxel-based-morphometry analysis to investigate the possible effect of the APOE epsilon4 gene on the gray matter. RESULTS: We found that the volume of the CC and all subregions decreased with increasing age in both groups. The slope was steeper in the APOE epsilon4 carriers compared withthe noncarriers particularly in the prefrontal region (P = 0.02). No gray matter differences were observed between the two groups. CONCLUSION: APOE epsilon4 polymorphism is associated with accelerated age-related volume loss in the prefrontal callosal tracts without gray matter loss. This result suggests the role of APOE epsilon4 in the brain aging by primarily affecting white matter structures particularly in the frontal lobe.

Pievani M, Rasser PE, Galluzzi S, Benussi L, Ghidoni R, Sabattoli F, Bonetti M, Binetti G, Thompson PM, Frisoni GB. · LENITEM Laboratory of Epidemiology, Neuroimaging and Telemedicine, IRCCS Centro San Giovanni di Dio - FBF, Brescia, Italy. · Neuroimage. · Pubmed #19349226 No free full text.

Abstract: Previous studies suggest that in Alzheimer's disease (AD) the Apolipoprotein E (APOE) epsilon4 allele is associated with greater vulnerability of medial temporal lobe structures. However, less is known about its effect on the whole cortical mantle. Here we aimed to identify APOE-related patterns of cortical atrophy in AD using an advanced computational anatomy technique. We studied 15 AD patients carriers (epsilon4+, age: 72+/-10 SD years, MMSE: 20+/-3 SD) and 14 non-carriers (epsilon4-, age: 69+/-9, MMSE: 20+/-5) of the epsilon4 allele and compared them to 29 age-and-sex matched controls (age: 70+/-9, MMSE: 28+/-1). Each subject underwent a clinical evaluation, a neuropsychological battery, and high-resolution MRI. UCLA's cortical pattern matching technique was used to identify regions of local cortical atrophy. epsilon4+ and epsilon4- patients showed similar performance on neuropsychological tests (p>.05, t-test). Diffuse cortical atrophy was detected for both epsilon4+ (p=.0001, permutation test) and epsilon4- patients (p=.0001, permutation test) relative to controls, and overall gray matter loss was about 15% in each patients group. Differences in gray matter loss between carriers and non-carriers mapped to the temporal cortex and right occipital pole (20% greater loss in carriers) and to the posterior cingulate, left orbitofrontal and dorsal fronto-parietal cortex (5-15% greater loss in non-carriers). APOE effect in AD was not significant (p>.74, ANOVA), but a significant APOE by region (temporal vs fronto-parietal cortex) interaction was detected (p=.002, ANOVA), in both early and late-onset patients (p<.05, ANOVA). We conclude that the epsilon4 allele modulates disease phenotype in AD, being associated with a pattern of differential temporal and fronto-parietal vulnerability.

Babiloni C, Frisoni GB, Del Percio C, Zanetti O, Bonomini C, Cassetta E, Pasqualetti P, Miniussi C, De Rosas M, Valenzano A, Cibelli G, Eusebi F, Rossini PM. · Department of Biomedical Sciences, University of Foggia, Viale Pinto 7, Foggia I-71100, Italy. · Clin Neurophysiol. · Pubmed #19324592 No free full text.

Abstract: OBJECTIVE: Non-steroidal anti-inflammatory drugs such as ibuprofen have a protective role on risk of Alzheimer's disease (AD). Here we evaluated the hypothesis that long-term ibuprofen treatment affects cortical sources of resting electroencephalographic (EEG) rhythms in mild AD patients. METHODS: Twenty-three AD patients (13 treated AD IBUPROFEN; 10 untreated AD PLACEBO) were enrolled. Resting EEG data were recorded before and 1 year after the ibuprofen/placebo treatment. EEG rhythms were delta (2-4 Hz), theta (4-8 Hz), alpha 1 (8-10.5 Hz), alpha 2 (10.5-13 Hz), beta 1 (13-20 Hz), and beta 2 (20-30 Hz). LORETA was used for EEG source analysis. RESULTS: In the AD PLACEBO group, amplitude of delta sources was globally greater at follow-up than baseline. Instead, amplitude of delta sources remained stable or decreased in the majority of the AD IBUPROFEN patients. Clinical (CDR) but not global cognitive status (MMSE) reflected EEG results. CONCLUSIONS: These results suggest that in mild AD patients, a long-term ibuprofen treatment slightly slows down the progressive increment of delta rhythms as a sign of contrast against the neurodegenerative processes. SIGNIFICANCE: They motivate future investigations with larger population and extended neuropsychological testing, to study the relationships among ibuprofen treatment, delta cortical sources, and higher order functions.

Geroldi C, Canu E, Bruni AC, Dal Forno G, Ferri R, Gabelli C, Perri R, Iapaolo D, Scarpino O, Sinforiani E, Zanetti O, Frisoni GB. · Laboratory of Epidemiology, Neuroimaging and Telemedicine, Scientific Institute for Research and Care (IRCCS) San Giovanni di Dio, FBF, Brescia, Italy. · Alzheimer Dis Assoc Disord. · Pubmed #19068498 No free full text.

Abstract: Aim of the study was to assess the added diagnostic value of neuropsychologic tests and structural neuroimaging (computed tomography or magnetic resonance) in the routine clinical assessment of demented patients in Italian expert centers. Nine centers were involved, located across the whole country (3 in Northern, 3 in Central, and 3 in Southern Italy). Diagnostic pathways were tracked for 474 patients with an expert diagnosis of neurodegenerative or vascular dementia (age 76+/-8; 62% females; Mini-Mental State Examination 17.70+/-5.7). The contribution of neuropsychology and structural neuroimaging to diagnosis was estimated as "number needed to test" (NNT), denoting the number of patients who need to undergo such procedures to improve expert diagnosis of 1 unit. Expert physicians reached their diagnosis without resorting to structural imaging examinations and neuropsychologic tests in 93% of Alzheimer disease (AD) and 76% of non-AD dementias. The completion of the extended assessment led to improvement of diagnostic accuracy in both cases: the NNT was 15.3 (95% confidence interval: 10.4-29.1) and 4.1 (3.0 to 6.5) for AD and non-AD diagnoses. The added value of structural imaging and neuropsychologic testing in the routine clinical assessment of demented patients is substantial in both AD and non-AD cases.

Winblad B, Frisoni GB, Frolich L, Johannsen P, Johansson G, Kehoe P, Lovestone S, Olde-Rikkert M, Reynish E, Visser PJ, Vellas B. · B. Winblad, Karolinska Institute - Alzheimer Disease Research Center, Stockholm, Sweden. · J Nutr Health Aging. · Pubmed #19043641 No free full text.

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Frisoni GB, Ganzola R, Canu E, Rüb U, Pizzini FB, Alessandrini F, Zoccatelli G, Beltramello A, Caltagirone C, Thompson PM. · Laboratory of Epidemiology Neuroimaging & Telemedicine, IRCCS Centro San Giovanni di Dio FBF, The National Centre for Research and Care of Alzheimer's and Mental Diseases, Brescia, Italy. · Brain. · Pubmed #18988639 No free full text.

Abstract: Histological studies have suggested differing involvement of the hippocampal subfields in ageing and in Alzheimer's disease. The aim of this study was to assess in vivo local hippocampal changes in ageing and Alzheimer's disease based on high resolution MRI at 3 Tesla. T(1)-weighted images were acquired from 19 Alzheimer's disease patients [age 76 +/- 6 years, three males, Mini-Mental State Examination 13 +/- 4] and 19 controls (age 74 +/- 5 years, 11 males, Mini-Mental State Examination 29 +/- 1). The hippocampal formation was isolated by manual tracing. Radial atrophy mapping was used to assess group differences and correlations by averaging hippocampal shapes across subjects using 3D parametric surface mesh models. Percentage difference, Pearson's r, and significance maps were produced. Hippocampal volumes were inversely correlated with age in older healthy controls (r = 0.56 and 0.6 to the right and left, respectively, P < 0.05, corresponding to 14% lower volume for every 10 years of older age from ages 65 to 85 years). Ageing-associated atrophy mapped to medial and lateral areas of the tail and body corresponding to the CA1 subfield and ventral areas of the head corresponding to the presubiculum. Significantly increased volume with older age mapped to a few small spots mainly located to the CA1 sector of the right hippocampus. Volumes were 35% and 30% smaller in Alzheimer's disease patients to the right and left (P < 0.0005). Alzheimer's disease-associated atrophy mapped not only to CA1 areas of the body and tail corresponding to those also associated with age, but also to dorsal CA1 areas of the head unaffected by age. Regions corresponding to the CA2-3 fields were relatively spared in both ageing and Alzheimer's disease. Hippocampal atrophy in Alzheimer's disease maps to areas in the body and tail that partly overlap those affected by normal ageing. Specific areas in the anterior and dorsal CA1 subfield involved in Alzheimer's disease were not in normal ageing. These patterns might relate to differential neural systems involved in Alzheimer's disease and ageing.