MRI线性测量局部脑萎缩对早期阿尔兹海默病的诊断意义

目的评价ＭＲＩ线性测量脑萎缩程度对阿尔兹海默病（Ａｌｚｈｅｉｍｅｒｄｉｓｅａｓｅ，ＡＤ）患者的早期诊断价值。方法应用ＭＲＩ线性定量测量对３０例轻度痴呆的ＡＤ患者、２０例多发脑梗塞性痴呆（ＭＩＤ）和２０名正常老年人进行局部额叶（双额指数、额叶半球间宽度）、中颞叶（海马钩回间距、中颞叶最小厚度）及海马结构（海马高度、脉络膜裂宽度、海马脑干间距及颞角宽度）等指标测量。结果颞角宽度指标是区别ＡＤ患者与ＭＩＤ患者及正常老年人的最敏感的指标；其敏感性达９０％，特异性达８５％。如结合脉络膜裂宽度、海马高度、海马与脑干间距及海马钩回间距，其敏感性达９３％，特异性达９５％。结论ＭＲＩ线性定量测量局部海马萎缩能够作为早期诊断ＡＤ的准确可靠性指标之一。     

Assessing the onset of structural change in familial Alzheimer's disease

Regional and global cerebral atrophy are inevitable features of Alzheimer's disease (AD). We assessed volumes and atrophy rates of brain structures in patients with familial AD during the period that they developed symptoms. Five patients with presymptomatic AD and 20 controls had two or more annual volumetric MRI brain scans. Volumes of brain, ventricles, temporal lobes, hippocampi, and entorhinal cortices (ECs) were measured. Rates of volume change were calculated from serial scans. There were no significant differences in baseline measures of whole brain, temporal lobe, or ventricular volume between patients and controls; averaged volumes of medial temporal lobe structures (both hippocampi and ECs) were 16.6% (95% confidence interval [CI], 3.3-28.0%) lower in patients. Atrophy rates for brain, temporal lobe, hippocampus, and EC were significantly increased in patients compared with controls (p < 0.05). Averaged atrophy rates from both hippocampi and ECs were 5.1% (95% CI, 3.0-7.1%) greater in patients than controls. Linear extrapolation backward suggested medial temporal lobe atrophy commenced 3.5 years (95% CI, 0.7-7.5 years) before onset, when all patients were asymptomatic. We conclude that increased medial temporal lobe atrophy rates are an early and distinguishing feature of AD and that pathological atrophy probably is occurring several years before the onset of symptoms.     

The Radial Width of the Temporal Horn in Mild Cognitive Impairment

BACKGROUND AND PURPOSE: The diagnosis of preclinical Alzheimer's disease (AD) (or mild cognitive impairment [MCI]) is loaded with a high degree of uncertainty. The aim was to test the accuracy of a computed tomography-based (CT-based) marker of medial temporal lobe atrophy, the radial width of the temporal horn (rWTH), in MCI. METHODS: Ten MCI and 42 AD patients and 29 nondemented controls underwent brain CT on the temporal lobe plane (slice thickness = 2 mm). The rWTH was taken on CT films with a precision caliper placed at the tip of the temporal horn radial to the curvature of the hippocampal head region. RESULTS: When specificity was fixed at 95%, the sensitivity for the detection of AD was 39/42 (93%) and that for the detection of MCI was 8/10 (80%). CONCLUSION: The rWTH is a measure sensitive to the regional brain atrophy common in early AD.     

Magnetic resonance measures in Alzheimer disease: their utility in early diagnosis and evaluating disease progression.

We sought to identify the most reliable magnetic resonance (MR) measures for the diagnosis and staging of Alzheimer disease (AD) in a clinical setting and to estimate, for different degrees of dementia, the rate of change of cerebral atrophy in certain regions of interest (ROIs). Forty-two probable AD patients and eight normal controls underwent MR brain scans, neurological examinations, and neuropsychological testing. We computed each subject's corpus callosum width, ventricular size, right and left temporal lobe areas, interuncal distance, and assessed the degree of cortical atrophy. We also estimated the rate of change for Information-Memory-Concentration Test scores and for temporal lobe areas and corpus callosum width. Measures of temporal lobe area and subjective evaluation of temporal lobe atrophy both served to distinguish controls from mild AD cases (p < 0.05), whereas only the latter differentiated moderate from severe patients (p < 0.05). The rate of change for temporal lobe areas remained constant over different AD stages, whereas those for corpus callosum width and for cognitive impairment were greater for severe cases (p < 0.05). Our findings imply that measurements of temporal lobe area and ratings of temporoparietal atrophy can be useful in the diagnosis and staging of AD and suggest that atrophy progressed at different rates in selected ROIs for various stages of AD severity.     

Rates of global and regional cerebral atrophy in AD and frontotemporal dementia.

OBJECTIVE: Serial registered MRI provides a reproducible technique for detecting progressive cerebral atrophy in vivo and was used to determine if there were differences between the rates of cerebral atrophy in AD and frontotemporal dementia (FTD). METHODS: Eighty-four patients with dementia (54 AD and 30 FTD) and 27 age-matched control subjects each had at least two volumetric MR scans. Serial scans were positionally matched (registered), and brain volume loss was determined by calculation of the brain boundary shift integral. RESULTS: There was a difference between the rates of whole-brain atrophy in patients (mean annual volume loss 2.7% of total brain volume) and in control subjects (mean annual volume loss 0.5%). AD and FTD were associated with different rates of atrophy (mean annual losses 2.4 and 3.2%). The range of atrophy rates in the FTD group (0.3 to 8.0%) greatly exceeded that in the AD group (0.5 to 4.7%). Frontal-variant FTD was associated with a wider range of atrophy rates than temporal-variant FTD. Analysis of regional brain atrophy rates revealed that there was widespread symmetrically distributed cerebral volume loss in AD, whereas in frontal FTD there was greater atrophy anteriorly and in temporal FTD the atrophy rate was greatest in the left anterior cerebral cortex. CONCLUSIONS: Both AD and FTD patients had increased rates of brain atrophy. Whereas the patients with AD were associated with a relatively restricted spread of atrophy rates, the greater spread of rates observed in the patients with FTD may reflect the heterogeneity of disease in FTD, with differences observed between frontal and temporal FTD. Increased rates of whole-brain atrophy did not discriminate AD from FTD, but analysis of regional atrophy rates revealed marked differences between patient groups.     

Neuroimaging as a marker of the onset and progression of Alzheimer's disease

Several neuroimaging techniques are promising tools as early markers of brain pathology in Alzheimer's disease (AD). On structural MRI, atrophy of the entorhinal cortex is present already in mild cognitive impairment (MCI). In the autosomal dominant forms of AD, the rate of atrophy of medial temporal structures separates affected from control persons even 3 years before the clinical onset of cognitive impairment. The elevated annual rate of brain atrophy offers a surrogate tool for the evaluation of newer therapies using smaller samples, thereby saving time and resources. On functional MRI, activation paradigms activate a larger area of parieto-temporal association cortex in persons at higher risk for AD, whereas the entorhinal cortex activation is lesser in MCI. Similar findings have been detected with activation procedures and water (H(2)(15)O) PET. Regional metabolism in the entorhinal cortex, studied with FDG PET, seems to predict normal elderly who will deteriorate to MCI or AD. SPECT shows decreased regional perfusion in limbic areas, both in MCI and AD, but with a lower likelihood ratio than PET. Newer PET compounds allow for the determination in AD of microglial activation, regional deposition of amyloid and the evaluation of enzymatic activity in the brain of AD patients.     

Early-onset versus late-onset Alzheimer's disease: the case of the missing APOE ɛ4 allele

Some patients with early-onset Alzheimer's disease (AD) present with a distinct phenotype. Typically, the first and most salient characteristic of AD is episodic memory impairment. A few patients, however, present with focal cortical, non-memory symptoms, such as difficulties with language, visuospatial, or executive functions. These presentations are associated with specific patterns of atrophy and frequently with a young age at onset. Age is not, however, the only determinant of phenotype; underlying factors, especially genetic factors, seem also to affect phenotype and predispose patients to younger or older age at onset. Importantly, patients with atypical early-onset disease seldom carry the APOE ?4 allele, which is the most important risk factor for lowering the age of onset in patients with AD. Additionally, theAPOE ?4 genotype seems to predispose patients to vulnerability in the medial temporal areas, which leads to memory loss. Conversely, patients negative for the APOE ?4 allele and with early-onset AD are more likely to be predisposed to vulnerability of cerebral networks beyond the medial temporal lobes. Other factors are probably involved in determining the pattern of atrophy, but these are currently unknown.     

The CT-based radial width of the temporal horn: pathological validation in AD without cerebrovascular disease

BACKGROUND: Medial temporal lobe atrophy is one of the most accurate markers of Alzheimer's disease (AD). Given the wide availability of the CT in the routine diagnostic assessment of patients with cognitive disturbances, a CT-based marker of AD might be clinically useful. OBJECTIVE: To test the accuracy of a simple CT-based measure, the radial width of the temporal horn (rWTH). METHOD: The rWTH was taken in a group of 20 pathologically confirmed AD patients and 23 non demented persons enrolled in the Oxford Project to Investigate Memory and Aging (OPTIMA project). RESULTS: The rWTH was significantly larger in AD patients than controls. Using a cutoff value between 3.9 at 50 and 8.1 at 90 years, the rWTH was able to correctly classify 16/20 and 19/23 subjects with a sensitivity and a specificity of 80% and 83%. The overall accuracy was 81%. CONCLUSION: The CT measurement of the rWTH is a simple and reasonably sensitive marker of regional brain atrophy in AD.     

The effect of brain atrophy on cerebral hypometabolism in the visual variant of Alzheimer disease

BACKGROUND: Brain glucose metabolic rates measured by positron emission tomography can be more affected by partial volume effects in Alzheimer disease (AD) than in healthy aging because of disease-associated brain atrophy. OBJECTIVE: To determine whether the distinct distribution of cerebral metabolic lesions in patients with the visual variant of AD (AD + VS) represents a true index of neuronal/synaptic dysfunction or is the consequence of brain atrophy. SETTING: Government research hospital. DESIGN: Resting cerebral metabolic rate for glucose was measured with positron emission tomography in a cross-sectional study of AD and AD + VS groups and in healthy control subjects. Segmented magnetic resonance images were used to correct for brain atrophy. PATIENTS: Patients with AD + VS had prominent visual and visuospatial symptoms. There were 15 patients with AD, 10 with AD + VS, and 37 age-matched control subjects. MAIN OUTCOME MEASURE: Measurement of the rate of cerebral glucose metabolism. RESULTS: Before atrophy correction, the AD + VS group, compared with the control subjects, showed hypometabolism in primary and extrastriate visual areas and in parietal and superior temporal cortical areas. Compared with the AD group, the AD + VS group showed hypometabolism in visual association areas. After atrophy correction, hypometabolism remained significantly different between patients and controls and between the 2 AD groups. CONCLUSIONS: The reductions in cerebral hypometabolism represent a true loss of functional activity and are not simply an artifact caused by brain atrophy. The different patterns of hypometabolism indicate the differential development of the lesions between the AD and AD + VS groups.     

Cognitive reserve modulates task-induced activations and deactivations in healthy elders, amnestic mild cognitive impairment and mild Alzheimer's disease

Introduction

Cognitive reserve (CR) reflects the capacity of the brain to endure neuropathology in order to minimize clinical manifestations. Previous studies showed that CR modulates the patterns of brain activity in both healthy and clinical populations. In the present study we sought to determine whether reorganizations of functional brain resources linked to CR could already be observed in amnestic mild cognitive impairment (a-MCI) and mild Alzheimer's disease (AD) patients when performing a task corresponding to an unaffected cognitive domain. We further investigated if activity in regions showing task-induced deactivations, usually identified as pertaining to the default-mode network (DMN), was also influenced by CR.

Methods

Fifteen healthy elders, 15 a-MCI and 15 AD patients underwent functional magnetic resonance imaging (fMRI) during a speech comprehension task. Differences in the regression of slopes between CR proxies and blood-oxygen-level dependent (BOLD) signals across clinical groups were investigated for activation and deactivation areas. Correlations between significant fMRI results and a language comprehension test were also computed.

Results

Among a-MCI and AD we observed positive correlations between CR measures and BOLD signals in task-induced activation areas directly processing speech, as well as greater deactivations in regions of the DMN. These relationships were inverted in healthy elders. We found no evidence that these results were mediated by gray matter volumes. Increased activity in left frontal areas and decreased activity in the anterior cingulate were related to better language comprehension in clinical evaluations.

Conclusions

The present findings provide evidence that the neurofunctional reorganizations related to CR among a-MCI and AD patients can be seen even when considering a preserved cognitive domain, being independent of gray matter atrophy. Areas showing both task-induced activations and deactivations are modulated by CR in an opposite manner when considering healthy elders versus patients. Brain reorganizations facilitated by CR may reflect behavioral compensatory mechanisms.     

Regional brain atrophy in patients with mild Alzheimer's disease and delusions

BACKGROUND AND OBJECTIVE: The pathophysiology and the neurobiology of the behavioral disturbances in Alzheimer's disease (AD) are far from understood. The aim of the study was to assess whether delusional AD patients have a specific pattern of regional brain atrophy. METHODS: The setting of the study was the outpatient facility of a memory clinic. Subjects were 41 AD patients with mild dementia severity (Mini-Mental State Exam score of 22 +/- 3, range 18 to 27). Delusions were assessed with the pertinent subscale of the UCLA Neuropsychiatric Inventory (NPI). Nondelusional (n = 22) AD and delusional (n = 19) AD were defined on the basis of absence (NPI delusions subscale = 0) or presence (NPI delusions subscale = 1 or higher) of delusions. Thirteen (68%) of the delusional patients had isolated theft delusions, and 6 (32%) had theft associated with another paranoid delusion (of jealousy or persecution). None of the patients had misidentifications or other delusions of nonparanoid content. Temporal lobe and frontal lobe atrophy were assessed with linear measures (radial width of the temporal horn, rWTH, and frontal index, FI) taken from computed tomographic films. Temporal and frontal asymmetries were computed as right/left ratio of the rWTH and FI. RESULTS: AD patients without delusions had symmetrical enlargement of both temporal (8.1 +/- 3.9 vs. 8.5 +/- 4.5) and frontal horns (35.8 +/- 4.8 vs. 35.9 +/- 4.6). On the contrary, AD with delusions showed temporal horns larger to the right (9.1 +/- 3.3 vs. 7.7 +/- 3.1, p = .06) and the frontal horn to the left (35.7 +/- 4.3 vs. 37.5 +/- 4.2, p = .02). This different pattern was confirmed with a gender-adjusted repeated measures analysis of variance model interaction term between asymmetry and group: F1,38 = 5.5, p = .03). DISCUSSION: AD patients with delusions are characterized by a specific pattern of frontal and temporal asymmetry of brain atrophy, whereas nondelusional patients are symmetric. Because the asymmetry pattern of the delusional patients is similar to the physiological pattern of asymmetry of individuals without dementia, the data indicate that the absence of theft delusions in the mild stage of AD rather than their presence is associated with an abnormal asymmetry pattern.     

Do cognitive patterns of brain magnetic activity correlate with hippocampal atrophy in Alzheimer's disease?

BACKGROUND: Many reports support the clinical validity of volumetric MRI measurements in Alzheimer's disease. OBJECTIVE: To integrate functional brain imaging data derived from magnetoencephalography (MEG) and volumetric data in patients with Alzheimer's disease and in age matched controls. METHODS: MEG data were obtained in the context of a probe-letter memory task. Volumetric measurements were obtained for lateral and mesial temporal lobe regions. RESULTS: As expected, Alzheimer's disease patients showed greater hippocampal atrophy than controls bilaterally. MEG derived indices of the degree of activation in left parietal and temporal lobe areas, occurring after 400 ms from stimulus onset, correlated significantly with the relative volume of lateral and mesial temporal regions. In addition, the size of the right hippocampus accounted for a significant portion of the variance in cognitive scores independently of brain activity measures. CONCLUSIONS: These data support the view that there is a relation between hippocampal atrophy and the degree of neurophysiological activity in the left temporal lobe.     

Magnetization transfer imaging in normal aging,mild cognitive impairment,and Alzheimer's disease

The purpose of this study was to assess whether structural brain damage as detected by volumetric magnetization transfer imaging (MTI) is present in mild cognitive impairment (MCI) and Alzheimer's disease (AD) and, if so, whether these abnormalities are global in character or restricted to the temporal lobe. Volumetric MTI analysis of the whole brain and temporal and frontal lobes was performed in 25 patients with probable AD, in 13 patients with MCI, and in 28 controls. Magnetization transfer ratio (MTR) histograms were produced, from which we derived measures for structural brain damage and atrophy. The peak heights of the MTR histograms of MCI and AD patients were lower than those of controls for the whole brain and temporal and frontal lobes, reflecting structural brain damage. AD patients had more atrophy than controls in all regions that were studied. MCI patients differed from controls for temporal lobe atrophy only. Volumetric MTI demonstrates structural changes that are related to cognitive decline in large parts of the brain of AD patients. Moreover, structural changes also were observed in MCI patients, indicating that widespread brain damage can be demonstrated before patients are clinically demented.     

Three-dimensional gray matter atrophy mapping in mild cognitive impairment and mild Alzheimer disease

BACKGROUND: Alzheimer disease (AD) is the most common form of dementia worldwide. Mild cognitive impairment (MCI) is the recent terminology for patients with cognitive deficiencies in the absence of functional decline. Most patients with MCI harbor the pathologic changes of AD and demonstrate transition to dementia at a rate of 10% to 15% per year. Patients with AD and MCI experience progressive brain atrophy. OBJECTIVE: To analyze the structural magnetic resonance imaging data for 24 patients with amnestic MCI and 25 patients with mild AD using an advanced 3-dimensional cortical mapping technique. DESIGN: Cross-sectional cohort design. Patients/ METHODS: We analyzed the structural magnetic resonance imaging data of 24 amnestic MCI (mean MMSE, 28.1; SD, 1.7) and 25 mild AD patients (all MMSE scores, >18; mean MMSE, 23.7; SD, 2.9) using an advanced 3-dimensional cortical mapping technique. RESULTS: We observed significantly greater cortical atrophy in patients with mild AD. The entorhinal cortex, right more than left lateral temporal cortex, right parietal cortex, and bilateral precuneus showed 15% more atrophy and the remainder of the cortex primarily exhibited 10% to 15% more atrophy in patients with mild AD than in patients with amnestic MCI. CONCLUSION: There are striking cortical differences between mild AD and the immediately preceding cognitive state of amnestic MCI. Cortical areas affected earlier in the disease process are more severely affected than those that are affected late. Our method may prove to be a reliable in vivo disease-tracking technique that can also be used for evaluating disease-modifying therapies in the future.     

Topographical patterns of lobar atrophy in frontotemporal dementia and Alzheimer's disease

BACKGROUND/AIMS: Fronto-temporal dementia (FTD) designates a group of relatively common neurodegenerative disorders. The aim of this study was to characterize the patterns of brain atrophy in FTD compared to Alzheimer's disease (AD). METHODS: A novel semiautomatic volumetric MRI analysis method was applied to measure regional brain volumes in FTD (n = 15; behavioural variant n = 9, language variant n = 6) in contrast with AD patients (n = 15) and age-matched controls (NC) (n = 15). FTD and AD patients were matched on demographic measures and Mini Mental State Examination scores. RESULTS: Significant atrophy was present in the frontal and anterior temporal lobes of subjects with FTD compared to AD (p = 0.02; effect size = 1.11) and compared to NC (p < 0.001; effect size = 1.86). Severe atrophy of the left anterior temporal region distinguished the language variant. AD patients, by contrast, did not differ from NC for frontal lobe volume but had smaller anterior temporal lobes (p = 0.03). Both dementia groups had medial temporal lobe atrophy of similar magnitude. A logistic regression model including 4 regional measures correctly classified 100% of subjects. CONCLUSION: FTD can be reliably differentiated from AD by virtue of a topographical pattern of atrophy involving the frontal lobes and anterior temporal regions. Medial temporal lobe volumes do not distinguish FTD from AD.     

Comparisons between global and focal brain atrophy rates in normal aging and Alzheimer disease: Boundary Shift Integral versus tracing of the entorhinal cortex and hippocampus

The objectives of this study were to (1) compare atrophy rates associated with normal aging and Alzheimer disease (AD) using the semi-automated Boundary Shift Integral (BSI) method and manual tracing of the entorhinal cortex (ERC) and hippocampus and (2) calculate power of BSI vs. ERC and hippocampal volume changes for clinical trials in AD. We quantified whole brain and ventricular BSI atrophy rates and ERC and hippocampal atrophy rates from longitudinal MRI data in 20 AD patients and 22 age-matched healthy controls. All methods revealed significant brain atrophy in controls and AD patients. AD patients had approximately 2.5 times greater whole brain BSI atrophy rates and more than 5 times greater ERC and hippocampal atrophy rates than controls. ERC and hippocampal atrophy rates were higher in both groups than whole brain BSI atrophy rates, but lower than ventricular BSI atrophy rates. Effect size and power calculations suggest that ERC and hippocampal measurements may be more sensitive than ventricular or whole brain BSI for detecting AD progression and the potential effects of disease modifying agents. Logistic regression analysis revealed that combined rates of ERC and ventricular BSI were the best explanatory variables for classifying AD from controls.     

Intracranial volume and Alzheimer disease: evidence against the cerebral reserve hypothesis

BACKGROUND: Total intracranial volume (TIV) measurement commonly is used to correct for variations in premorbid brain size in imaging studies of cerebral structures in Alzheimer disease (AD). This assumes no intrinsic difference in TIV between patients and control subjects and that TIV measurements are unaffected by cerebral atrophy. However, an autopsy study has suggested that a larger premorbid brain may protect against AD onset. A recent computed tomographic study lent support to this by finding a correlation between intracranial size and age at onset of AD in women. OBJECTIVE: To investigate the relationship between TIV and sporadic and familial AD. DESIGN: Retrospective case study. SETTING: Specialist dementia clinic. PATIENTS: Eighty-five patients with AD and 52 healthy volunteers. MAIN OUTCOME MEASURES: Age at symptom onset and TIV measured using a semiautomatic interactive thresholding technique on magnetic resonance imaging spanning the entire intracranial cavity. RESULTS: Reproducibility measurement was high (intrarater coefficient of variation, 1.2%; interrater coefficient of variation, 0.7%). Unlike brain atrophy in the patients with AD, TIV did not vary over time. Mean TIV did not differ significantly between any of the subject groups. There was no association between TIV and age or age at symptom onset. The only significant predictor of TIV was sex. CONCLUSIONS: Measurements of TIV are independent of atrophy and can be used safely to adjust for differences in head size in studies of cerebral structure in AD. Premorbid brain size does not differ between patients with familial and sporadic AD and controls and does not delay disease onset.     

Relationship of medial temporal lobe atrophy,APOE genotype,and cognitive reserve in preclinical Alzheimer's disease

This study evaluated the utility of baseline and longitudinal magnetic resonance imaging (MRI) measures of medial temporal lobe brain regions collected when participants were cognitively normal and largely in middle age (mean age 57 years) to predict the time to onset of clinical symptoms associated with mild cognitive impairment (MCI). Furthermore, we examined whether the relationship between MRI measures and clinical symptom onset was modified by apolipoprotein E (ApoE) genotype and level of cognitive reserve (CR). MRI scans and measures of CR were obtained at baseline from 245 participants who had been followed for up to 18 years (mean follow‐up 11 years). A composite score based on reading, vocabulary, and years of education was used as an index of CR. Cox regression models showed that lower baseline volume of the right hippocampus and smaller baseline thickness of the right entorhinal cortex predicted the time to symptom onset independently of CR and ApoE‐?4 genotype, which also predicted the onset of symptoms. The atrophy rates of bilateral entorhinal cortex and amygdala volumes were also associated with time to symptom onset, independent of CR, ApoE genotype, and baseline volume. Only one measure, the left entorhinal cortex baseline volume, interacted with CR, such that smaller volumes predicted symptom onset only in individuals with lower CR. These results suggest that MRI measures of medial temporal atrophy, ApoE‐?4 genotype, and the protective effects of higher CR all predict the time to onset of symptoms associated with MCI in a largely independent, additive manner during the preclinical phase of Alzheimer's disease. Hum Brain Mapp 36:2826–2841, 2015. © 2015 Wiley Periodicals, Inc.     

Perfusion SPECT and FDG-PET

Both perfusion SPECT and FDG-PET provide images that closely reflect neuronal activity. There is a characteristic regional impairment in Alzheimer’s disease (AD) that involves mainly the temporo-parietal association cortices, mesial temporal structures and to a more variable degree also the frontal association cortex. This pattern of functional impairment can provide a biomarker for diagnosis of AD and other neurodegenerative dementias at the clinical stage of mild cognitive impairment, and for monitoring of progression. FDG-PET is quantitatively more accurate and thus better suited to multicenter studies than perfusion SPECT. Regional metabolic and blood flow changes are closely related to clinical symptoms, and most areas involved in these changes will also develop significant cortical atrophy. FDG-PET is complementary to amyloid PET, which targets a molecular marker that does not have a close relation to current symptoms. Current restrictions in the availability and cost of FDG-PET are being reduced, as oncological FDG-PET is being adopted as a standard clinical service in most countries. Limitations in the availability of trained staff should be overcome by training programs set up by professional organizations. Against the background of the development of new criteria for diagnosing AD before the onset of dementia, FDG-PET is expected to play an increasing role in diagnosing patients at an early stage of AD and in clinical trials of drugs aimed at preventing or delaying the onset of dementia.     

Distinct white matter injury associated with medial temporal lobe atrophy in Alzheimer's versus semantic dementia

This study aims at further understanding the distinct vulnerability of brain networks in Alzheimer's disease (AD) versus semantic dementia (SD) investigating the white matter injury associated with medial temporal lobe (MTL) atrophy in both conditions. Twenty‐six AD patients, twenty‐one SD patients, and thirty‐nine controls underwent a high‐resolution T1‐MRI scan allowing to obtain maps of grey matter volume and white matter density. A statistical conjunction approach was used to identify MTL regions showing grey matter atrophy in both patient groups. The relationship between this common grey matter atrophy and white matter density maps was then assessed within each patient group. Patterns of grey matter atrophy were distinct in AD and SD but included a common region in the MTL, encompassing the hippocampus and amygdala. This common atrophy was associated with alterations in different white matter areas in AD versus SD, mainly including the cingulum and corpus callosum in AD, while restricted to the temporal lobe — essentially the uncinate and inferior longitudinal fasciculi — in SD. Complementary analyses revealed that these relationships remained significant when controlling for global atrophy or disease severity. Overall, this study provides the first evidence that atrophy of the same MTL region is related to damage in distinct white matter fibers in AD and SD. These different patterns emphasize the vulnerability of distinct brain networks related to the MTL in these two disorders, which might underlie the discrepancy in their symptoms. These results further suggest differences between AD and SD in the neuropathological processes occurring in the MTL. Hum Brain Mapp 38:1791–1800, 2017. © 2017 Wiley Periodicals, Inc.