Lobe Atrophy Research Articles

Lobar Atrophy in Frontotemporal Dementia: Diagnostic and Prognostic Implications

We review the practical importance of lobar atrophy in frontotemporal dementia (FTD), for diagnosis and prognosis. We discuss specific patterns of frontotemporal atrophy that denote clinical and pathological subtypes of FTD (e.g. semantic dementia). We also discuss the unsatisfactory clinical experience of interpreting MRI scans in individual FTD cases, especially the behavioural presentations (without aphasic or motor impairments). This issue is explored by examining the FTD phenocopy concept. Lobar atrophy emerges as a key observation in defining behavioural FTD patients whose symptoms are likely to progress. In a situation where objective clinical data are few, we highlight the importance of applying caution before diagnosing FTD is the absence of visible brain atrophy.

A Brazilian family with hereditary inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia

Inclusion body myopathy associated with Paget disease and frontotemporal dementia (IBMPFD) is a progressive and usually misdiagnosed autosomal dominant disorder. It is clinically characterized by a triad of features: proximal and distal myopathy, early onset Paget disease of bone (PDB), and frontotemporal dementia (FTD). It is caused by missense mutations in the valosin-containing protein (VCP) gene. We describe here the clinical and molecular findings of the first Brazilian family identified with IBMPFD. Progressive myopathy affecting the limb girdles was detected by clinical examination followed by muscle biopsy and creatine kinase measurement. PDB was suggested after anatomopathological bone examination and FTD was diagnosed by clinical, neuropsychological and language evaluations. Brain magnetic resonance revealed severe atrophy of the anterior temporal lobes, including the hippocampi. A R93C mutation in VCP was detected by direct sequencing screening in subject W (age 62) and in his mother. Four more individuals diagnosed with "dementia" were reported in this family. We also present a comprehensive genotype-phenotype correlation analysis of mutations in VCP in 182 patients from 29 families described in the literature and show that while IBM is a conspicuously penetrant symptom, PDB has a lower penetrance when associated with mutations in the AAAD1 domain and FTD has a lower penetrance when associated with mutations in the Junction (L1-D1) domain. Furthermore, the R93C mutation is likely to be associated with the penetrance of all the clinical symptoms of the triad.

Childhood outcomes of neonates diagnosed with portal vein thrombosis

The study aims to determine childhood outcomes of neonates diagnosed with portal vein thrombosis (PVT). A retrospective chart review of neonates diagnosed with PVT who had documented follow up (physical examination, laboratory tests or ultrasonographic examination) at the age of 2 years or beyond was conducted. Data were available for 70 children (71% of eligible neonates) at a median age of 5 years (range 2-8 years). Physical examination was unremarkable in all who were examined (n= 68). Twenty-five children had liver functions assessed and only mild abnormalities were detected in nine children. Six of 25 patients tested for thrombophilia showed abnormalities. Thirty-seven children had ultrasonographic follow up. Left lobar atrophy (LLA) was noted in 20 children (16 had isolated LLA, two had LLA and splenomegaly, and two had LLA and portal hypertension). Five children who had normal ultrasound examinations at discharge had splenomegaly (two with additional finding of LLA) at follow up. Two children with portal hypertension diagnosed during neonatal period needed porta-caval shunting. Our results show that among patients, who had PVT as neonates, 28% still had asymptomatic LLA in childhood, 7% had slowly progressive splenomegaly and 3% required shunting because of progression of portal hypertension. Ultrasonographic follow up was the most sensitive method in detecting progression associated with neonatal PVT. Until more data are available, periodic long-term ultrasonographic follow up should be considered for neonates diagnosed with PVT.

Pathological correlates of frontotemporal lobar degeneration in the elderly

Frontotemporal lobar degeneration (FTLD) is generally recognised as a disorder with presenile onset (that is before 65years of age) with only occasional cases presenting later than this. We set out to determine what proportion of cases of FTLD had late onset of disease and whether such cases of FTLD had distinctive clinical and neuropathological features as compared to cases with presenile onset. Within a combined Manchester and Newcastle autopsy series of 117 cases with pathologically confirmed FTLD (109/117 cases also met Lund Manchester clinical criteria for FTLD), we identified 30 cases (onset age range 65-86years), comprising 25% of all FTLD cases ascertained in these two centres over a 25-year period. Neuropathologically, the 30 elderly cases presented features of several FTLD histological subgroups [FTLD-TDP (types 1, 2 and 3, 19 cases (63%)], FLTD-tau [MAPT, PiD and CBD, 10 cases (33%)] and FTLD-UPS (1 case), similar in range of phenotypes to that seen in the presenile group, though patients with MAPT, but not PGRN, mutation, or FUS pathology, were notably absent or fewer in the elderly group. Hippocampal sclerosis (HS) was present in 13/30 of the elderly FTLD cases (43%) compared with 14/79 (18%) (P=0.012) in the presenile FTLD patients. Lobar atrophy present in most of the younger patients was prominent in only 25% of the elderly subjects. Prospective and retrospective psychiatric and medical case note analysis showed that the majority of the elderly FTLD patients, like their younger counterparts, had behavioural features consistent with frontotemporal dementia. FTLD is common amongst elderly persons and all or most of the major clinical and histological subtypes present in younger individuals can be seen in the older group.

Phenotypic spectrum of patients with PLA2G6 mutation and PARK14 -linked parkinsonism

PLA2G6 is the causative gene for infantile neuroaxonal dystrophy, neurodegeneration associated with brain iron accumulation, and Karak syndrome. Based on previous reports, patients with PLA2G6 mutations could show axonal dystrophy, dystonia, dementia, and cerebellar signs. Recently, PLA2G6 was also reported as the causative gene for early-onset PARK14-linked dystonia-parkinsonism. To clarify the role of PLA2G6 mutation in parkinsonism, we conducted mutation analysis in 29 selected patients with very early-onset (≤ 30, mean 21.2 ± 8.4 years, ± SD) parkinsonism. These patients had other clinical features (e.g., mental retardation/dementia [14/29], psychosis [15/29], dystonia [11/29], and hyperreflexia [11/29]). Two novel compound heterozygous PLA2G6 mutations were detected (patient A: p.F72L/p.R635Q; patients B1 and B2: p.Q452X/p.R635Q). All 3 patients had early-onset l-dopa-responsive parkinsonism with dementia and frontotemporal lobar atrophy. Disease progression was relatively rapid. SPECT in patient B1 showed frontotemporal lobar hypoperfusion. MRI in patient A showed iron accumulation in the substantia nigra and striatum. Although the clinical presentation of PLA2G6-associated neurodegeneration was reported to be homogeneous, our findings suggest patients with PLA2G6 mutation could show heterogeneous phenotype such as dystonia-parkinsonism, dementia, frontotemporal atrophy/hypoperfusion, with or without brain iron accumulation. Based on the clinical heterogeneity, the functional roles of PLA2G6 and the roles of PLA2G6 variants including single heterozygous mutations should be further elucidated in patients with atypical parkinsonism, dementia, or Parkinson disease. PLA2G6 mutations should be considered in patients with early-onset l-dopa-responsive parkinsonism and dementia with frontotemporal lobar atrophy.

Hilar cholangiocarcinoma: MR correlation with surgical and histological findings

To evaluate magnetic resonance cholangiography (MRC) with high-resolution dynamic gadolinium-enhanced magnetic resonance imaging (MRI) in determining the imaging features of hilar cholangiocarcinoma that relate to tumour extent and influence resectability. Twenty-six patients that underwent resection were reviewed. Tumour location and extent, lobar atrophy, the degree of portal vein and hepatic artery involvement were recorded. The findings were correlated with surgical and histopathological findings. Biliary assessment was concordant in 14 and discordant in eight of 14 stented and four of 12 non-stented patients. In 63/82 veins and 43/74 arteries results were fully concordant. The mean sensitivity, specificity, positive and negative predictive values (PPV, NPV) in predicting involvement of the main portal vein (MPV) at surgery were 83.3, 100, 100, and 92.5%; of the left main branch of the portal vein (LPV) were 100, 91.6, 93.3, and 100%; and of the right branch of the portal vein (RPV) were 87.5, 100, 100, and 87.5%. The sensitivity, specificity, PPV and NPV of MRI in determining histological involvement of the MPV was 75, 90.9, 60, and 92.5%; 100, 73.3, 73, and 100% for the LPV, and 100, 66.6, 42.8, and 100% for the RPV, respectively. MRC with high-resolution dynamic gadolinium-enhanced MRI is effective in determining tumour extent and vascular involvement, but prior stenting may lead to overestimation.

Clinical Characteristics of Patients With Frontotemporal Dementia With and Without Lobar Atrophy on MRI

The presence of frontal and/or temporal atrophy on neuroimaging has been designated as supportive in the clinical consensus criteria for behavioral variant frontotemporal dementia (bvFTD). As magnetic resonance imaging (MRI) has a relatively low sensitivity for bvFTD, a substantial proportion of patients may present with a normal MRI. Thus, there may be clinical differences between patients with and without lobar abnormalities on MRI. We compared clinical characteristics of bvFTD patients with frontotemporal lobar atrophy on MRI to those lacking the typical pattern at presentation. MRIs of 49 patients from our memory clinic, diagnosed with bvFTD were rated for the presence or absence of frontal and/or temporal atrophy. Demographic, behavioral, and cognitive features were compared between subjects with and without typical bvFTD atrophy pattern. Twenty-three patients showed lobar atrophy on MRI, whereas 26 patients lacked the characteristic frontotemporal lobar atrophy, including 13 patients with a normal MRI and 13 with other abnormalities. Disinhibition occurred more often in the group with frontal and/or temporal atrophy on MRI compared with the group with other abnormalities, whereas imitation did not occur in patients lacking the typical bvFTD atrophy pattern. No differences were found in neuropsychologic profiles. There was a trend for a lower mean Clinical Dementia Rating and less severe language impairment in patients with a normal MRI compared with the group with frontal and/or temporal atrophy. The clinical phenotype of FTD cannot be predicted by the presence or absence of lobar atrophy on MRI, although imitation and disinhibition are more prevalent in bvFTD patients with characteristic MRI abnormalities. Furthermore, patients with a normal MRI seem to be less severely demented in comparison to patients with frontal and/or temporal atrophy.

Study on the Pathogenesis of Foreign Body Granulomatous Inflammation in the Livers of Sprague-Dawley Rats

Focal granulomatous inflammation developed in the livers of five 10-week-old male Sprague-Dawley rats. The characteristic features of this lesion were the presence of foreign body multinucleated giant cells engulfing calcium deposits and site-specific development in a fissure formed in a sub-lobation in the left lobe or interlobar fissure of the medial lobe of the liver. To clarify the pathogenesis of this lesion, rat livers showing abnormal sub-lobation or lobar atrophy, rat livers in an acute dermal toxicity study and guinea pig livers in a skin sensitization test were also examined histologically. Consequently, the present lesion was considered to be a reactive change against calcium that was dystrophically deposited in the area of hepatocellular necrosis due to delayed circulatory disturbance caused by external pressure or extension force. Granulomatous lesions like in the present cases should be differentiated from those caused by evident exogenous pathogens such as chemicals or microorganisms.

Does the brain prefer geometrical homogeneity?

Some patients with frontotemporal lobar degeneration (FTLD) have shown the development of painting or musical abilities after the onset of the disease. In this report, we present another emergent ability. A female patient with FTLD showing dense atrophy of the bilateral anterior lobes and a loss of voluntary activity in aspects of daily living, presented with the characteristic behaviours when given a paper and a pair of scissors. When a shape was already drawn on the paper, she showed reasonable skills with the scissors, cutting without any hesitation. When she cut a blank piece of paper, she showed quite unique geometrical preferences. Her severely degenerated brain combined with her geometrical abilities suggests that the human brain is naturally affected by geometrical homogeneity.

Two cases of frontotemporal dementia with predominant temporal lobe atrophy

Frontotemporal dementia (FTD) is a subtype of frontotemporal lobar degeneration, which also includes semantic dementia (SD) and progressive non-fluent aphasia. Frontotemporal dementia is characterized by changes in personality and behavioral abnormalities, generally associated with predominant frontal lobe atrophy. Conversely, SD is typically characterized by Gogi (word meaning) aphasia based on semantic memory impairment and is associated with predominant temporal lobe atrophy. However, in the present cases, we diagnosed FTD on the basis of clinical symptoms, such as disinhibition, indifference, and stereotypy, without semantic memory impairment, even though neuroimaging showed predominant temporal lobe atrophy. We suggest that clinical symptoms are the most important cues for an accurate clinical diagnosis and there is no exclusive relationship between the syndrome and atrophy of the temporal lobes.

Frontal lobe atrophy is associated with small vessel disease in ischemic stroke patients

Background The pathogenesis of frontal lobe atrophy (FLA) in stroke patients is unclear. We aimed to ascertain whether subcortical ischemic changes were more associated with FLA than with parietal lobe atrophy (PLA) and temporal lobe atrophy (TLA). Methods Brain magnetic resonance images (MRIs) from 471 Chinese ischemic stroke patients were analyzed. Lobar atrophy was defined by a widely used visual rating scale. All patients were divided into non-severe, mild–moderate, and severe atrophy of the frontal, parietal, and temporal lobe groups. The severity of white matter lesions (WMLs) was rated with the Fazekas’ scale. Clinical and radiological features were compared among the groups. Subsequent logistic regressions were performed to determine the risk factors of atrophy and severe atrophy of the frontal, parietal and temporal lobes. Results The frequency of FLA in our cohort was 36.9% (174/471). Severe FLA occurred in 30 (6.4%) patients. Age, previous stroke, and periventricular hyperintensities (PVH) (odds ratio (OR) = 1.640, p = 0.039) were independent risk factors of FLA. Age and deep white matter hyperintensities (DWMH) (OR = 3.634, p = 0.002) were independent risk factors of severe FLA. PVH and DWMH were not independent risk factors of PLA and TLA. Conclusion Frontal lobe atrophy in ischemic stroke patients may be associated with small vessel disease. The association between WMLs and FLA was predominant over atrophy of the parietal and temporal lobes, which suggests that the frontal lobe may be vulnerable to subcortical ischemic changes.

Role of preoperative biliary drainage of liver remnant prior to extended liver resection for hilar cholangiocarcinoma

BackgroundIn patients with hilar cholangiocarcinoma, ipsilateral en bloc hepatic resection improves survival but is associated with increased morbidity. Preoperative biliary drainage of the future liver remnant (FLR) and contralateral portal vein embolization (PVE) may improve perioperative outcome, but their routine use is controversial. This study analyses the impact of FLR volume and preoperative biliary drainage on postoperative hepatic insufficiency and mortality rates. MethodsPatients who underwent hepatic resection and for whom adequate imaging data for FLR calculation were available were identified retrospectively. Patient demographic, operative and perioperative data were recorded and analysed. The volume of the FLR was calculated based on the total liver volume and the volume of the resection that was actually performed using semi-automated contouring of the liver on preoperative helical acquired scans. In patients subjected to preoperative biliary drainage, the preoperative imaging was reviewed to determine if the FLR had been decompressed. Hepatic insufficiency was defined as a postoperative rise in bilirubin of 5mg/dl above the preoperative level that persisted for >5 days postoperatively. Operative mortality was defined as death related to the operation, whenever it occurred. ResultsSixty patients were identified who underwent hepatic resection between 1997 and 2007 and for whom imaging data were available for analysis. During this period, preoperative biliary drainage of the FLR was used selectively and PVE was used in only one patient. The mean age of the patients was 64 ± 11.6 years and 68% were male. The median length of stay was 14 days and the overall morbidity and mortality were 53% and 10%, respectively. Preoperative FLR volume was a predictor of hepatic insufficiency and death (P= 0.03). A total of 65% of patients had an FLR volume ≥30% (39/60) of the total volume. No patient in this group had hepatic insufficiency, but there were two operative deaths (5%), both occurring in patients who underwent preoperative biliary drainage. By contrast, in the group with FLR < 30% (21/60, 35%), hepatic insufficiency was seen in five patients and operative mortality in four patients, and were strongly associated with lack of preoperative biliary drainage of the FLR (P= 0.009). Patients with an FLR ≥ 30% were more likely to have radiographic evidence of ipsilateral lobar atrophy and hypertrophy of the FLR (46.2% vs. 9.5% in patients with FLR < 30%; P= 0.004). ConclusionsIn patients undergoing liver resection for hilar cholangiocarcinoma, FLR volume of < 30% of total liver volume is associated with increased risk for hepatic insufficiency and death. Preoperative biliary drainage of the FLR appears to improve outcome if the predicted volume is < 30%. However, in patients with FLR ≥ 30%, preoperative biliary drainage does not appear to improve perioperative outcome and, as many of these patients have hypertrophy of the FLR, PVE is likely to offer little benefit.

HDDD with Alzheimer's disease as common comorbidity: A clinicopathologic case report

Hereditary dysphasic disinhibition dementia (HDDD) describes a familial disorder characterized by personality changes, language and memory deficits. The neuropathology includes frontotemporal lobar atrophy, neuronal loss and gliosis and, in most cases abundant amyloid beta plaques and neuropibrillary tangles. A Pick/Alzheimer's spectrum was proposed for the original family HDDD1. Here we report the clinicopathologic case of an HDDD1 individual with additional Alzheimer's disease (AD) pathology, as a common comorbidity, which may mislead clinicians in diagnosis.

VCP Mutations Causing Frontotemporal Lobar Degeneration Disrupt Localization of TDP-43 and Induce Cell Death

Frontotemporal lobar degeneration (FTLD) with inclusion body myopathy and Paget disease of bone is a rare, autosomal dominant disorder caused by mutations in the VCP (valosin-containing protein) gene. The disease is characterized neuropathologically by frontal and temporal lobar atrophy, neuron loss and gliosis, and ubiquitin-positive inclusions (FTLD-U), which are distinct from those seen in other sporadic and familial FTLD-U entities. The major component of the ubiquitinated inclusions of FTLD with VCP mutation is TDP-43 (TAR DNA-binding protein of 43 kDa). TDP-43 proteinopathy links sporadic amyotrophic lateral sclerosis, sporadic FTLD-U, and most familial forms of FTLD-U. Understanding the relationship between individual gene defects and pathologic TDP-43 will facilitate the characterization of the mechanisms leading to neurodegeneration. Using cell culture models, we have investigated the role of mutant VCP in intracellular trafficking, proteasomal function, and cell death and demonstrate that mutations in the VCP gene 1) alter localization of TDP-43 between the nucleus and cytosol, 2) decrease proteasome activity, 3) induce endoplasmic reticulum stress, 4) increase markers of apoptosis, and 5) impair cell viability. These results suggest that VCP mutation-induced neurodegeneration is mediated by several mechanisms.

Radiation Lobectomy: Preliminary Findings of Hepatic Volumetric Response to Lobar Yttrium-90 Radioembolization

To describe volumetric changes of "radiation lobectomy," a manifestation of hepatic parenchymal response to lobar (90)Y microsphere radioembolization. Twenty patients exhibiting this phenomenon were identified. Pre- and posttreatment absolute right and left hepatic lobar volume (HLV), relative HLV (rHLV = HLV/total liver volume), and degree of lobar atrophy (DA) or hypertrophy (DH) (DA or DH = |posttreatment rHLV - pretreatment rHLV|) were determined. Laboratory toxicities, tumor response, and patient survival were also assessed. Twenty patients with primary (HCC, n = 17; peripheral cholangiocarcinoma, n = 3) liver malignancies demonstrated findings of radiation lobectomy. Initial absolute right and left HLV was 955 cm(3) (range 644-1,842 cm(3), rHLV = 57%) and 719 cm(3) (range 328-1,387 cm(3), rHLV = 43%), respectively. Following (90)Y, absolute right HLV decreased to 460 cm(3) (range 185-948 cm(3), 52% reduction, rHLV = 31%, DA = 26%, P < 0.0001), while absolute left HLV increased to 1,004 cm(3) (range 560-1,558 cm(3), 40% increase, rHLV = 69%, DH = 26%, P < 0.0001). No grade 3 or 4 bilirubin toxicities were encountered. Tumor response ranged from 55% to 70% by size criteria. Forty-six percent 5-year survival was achieved in HCC patients. Radiation lobectomy following (90)Y radioembolization of right lobe tumors manifests extensive contralateral lobar hypertrophy, high response rates, and prolonged survival. This phenomenon was noted in 6.4% (20/315) of the entire cohort and 19.8% (20/101) of patients with unilobar right lobe tumors. Further investigation is necessary to determine contributing factors that may predict this effect.

Neuroimaging findings in children with retinopathy-confirmed cerebral malaria

Purpose To describe brain CT findings in retinopathy-confirmed, paediatric cerebral malaria. Materials and methods In this outcomes study of paediatric cerebral malaria, a subset of children with protracted coma during initial presentation was scanned acutely. Survivors experiencing adverse neurological outcomes also underwent a head CT. All children had ophthalmological examination to confirm the presence of the retinopathy specific for cerebral malaria. Independent interpretation of CT images was provided by two neuroradiologists. Results Acute brain CT findings in three children included diffuse oedema with obstructive hydrocephalus (2), acute cerebral infarctions in multiple large vessel distributions with secondary oedema and herniation (1), and oedema of thalamic grey matter (1). One child who was reportedly normal prior to admission had parenchymal atrophy suggestive of pre-existing CNS injury. Among 56 survivors (9–84 months old), 15 had adverse neurologic outcomes—11/15 had a follow-up head CT, 3/15 died and 1/15 refused CT. Follow-up head CTs obtained 7–18 months after the acute infection revealed focal and multifocal lobar atrophy correlating to regions affected by focal seizures during the acute infection (5/11). Other findings were communicating hydrocephalus (2/11), vermian atrophy (1/11) and normal studies (3/11). Conclusions The identification of pre-existing imaging abnormalities in acute cerebral malaria suggests that population-based studies are required to establish the rate and nature of incidental imaging abnormalities in Malawi. Children with focal seizures during acute cerebral malaria developed focal cortical atrophy in these regions at follow-up. Longitudinal studies are needed to further elucidate mechanisms of CNS injury and death in this common fatal disease.

Progranulin plasma levels in the diagnosis of frontotemporal dementia.

Not so long ago many neurologists were trained to believe that Pick's disease was rare and usually impossible to differentiate accurately from Alzheimer's disease. Through the persistent efforts of several research groups, especially in Lund (Sweden) and Manchester (UK), it became clear that this ‘disease’ is not rare and can frequently be distinguished from Alzheimer's disease (Brun et al. , 1994). Now, this entity is better described as frontotemporal dementia (FTD) or frontotemporal lobar degeneration based on the frequent occurrence of lobar atrophy involving frontal and/or temporal lobes (Snowden et al. , 1996). And rather than constituting a single disease, FTD represents a group of overlapping disorders having different pathogenic mechanisms, some, but not all, of which have been identified. There are several different ways to subdivide the various types of FTD. One is to use clinical manifestations such as the behavioural or language variants (such as semantic dementia and many cases of primary progressive aphasia) and FTD associated with motor neuron disease. The second type of subdivision is made on the basis of neuropathological features. This …

Chemoembolic lobectomy: imaging findings of hepatic lobar volume reduction after transcatheter arterial chemoembolization

Hepatic lobar atrophy-hypertrophy complex formation is an uncommonly reported sequella of hepatic arterial embolotherapy procedures. Whereas radiation-induced hepatic lobar ablation has been described after intra-arterial therapy with yttrium-90 microspheres, this phenomenon has not been reported after transcatheter arterial chemoembolization. Here, we report a case of prominent hepatic lobar atrophy with contralateral lobar hypertrophy after chemoembolization and suggest a mechanism by which arterial embolization contributes to the volumetric response.

Experimental study of selective portal vein embolization with the mixture of ZT glue and lipiodol

Objective To evaluate the feasibility of Selective Portal Vein Embolization(SPVE)in rabbits with the mixture of ZT glue and Lipiodol.Methods Sixteen white New Zealand rabbits were randomly divided into 2 groups:Group A,ZT glue:Lipiodol(1:2)mixture and Group B Lipiodol group.SPVE of left branch was performed in each group under digital subtraction angiography.The distribution feature of the embolic agents and the histopathology of liver in each group were observed.The weight ratio of the right lobe to the whole liver at the 30th day after SPVE were recorded and analyzed.Results Permanent embolization were occurred in group A.Recanalization was appeared in group B.Atrophy of the embolized lobes and compensatory hypertrophy of none-embolized lohes was,observed..The weight ratio of the right lobe to the whole liver Was 69.41±5.10% in group A.There was statistical difference between these two groups(P＜0.05).Conclusion There were permanent embolization after SPVE with the mixture of ZT glue and lipiodol.SPVE induced atrophy of the embolized lobes of liver and compensatory hypertrophy of none-embolized lobes. Key words: Tissue adhesives/AD; Iodized oil/AD; Embolization,therapeutic; Portal vein

P2-017: Lobar gray and white matter atrophy in Alzheimer's Disease: Preliminary results from the ADNI public database

P2-017: Lobar gray and white matter atrophy in Alzheimer's Disease: Preliminary results from the ADNI public database