Database : MEDLINE
Search on : Neurodegenerative and Diseases [Words]
References found : 48876 [refine]
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[PMID]: 29524628
[Au] Autor:Gabriel Enge T; Ecroyd H; Jolley DF; Yerbury JJ; Kalmar B; Dosseto A
[Ad] Address:Wollongong Isotope Geochronology Laboratory and School of Earth and Environmental Sciences, University of Wollongong, Australia. Electronic address: tge571@uowmail.edu.au.
[Ti] Title:Assessment of metal concentrations in the SOD1 mouse model of amyotrophic lateral sclerosis and its potential role in muscular denervation, with particular focus on muscle tissue.
[So] Source:Mol Cell Neurosci;, 2018 Mar 07.
[Is] ISSN:1095-9327
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Amyotrophic lateral sclerosis (ALS) is among the most common of the motor neuron diseases, and arguably the most devastating. During the course of this fatal neurodegenerative disorder, motor neurons undergo progressive degeneration. The currently best-understood animal models of ALS are based on the over-expression of mutant isoforms of Cu/Zn superoxide dismutase 1 (SOD1); these indicate that there is a perturbation in metal homeostasis with disease progression. Copper metabolism in particular is affected in the central nervous system (CNS) and muscle tissue. METHODS: This present study assessed previously published and newly gathered concentrations of transition metals (Cu, Zn, Fe and Se) in CNS (brain and spinal cord) and non-CNS (liver, intestine, heart and muscle) tissues from transgenic mice over-expressing the G93A mutant SOD1 isoform (SOD1 ), transgenic mice over-expressing wildtype SOD1 (SOD1 ) and non-transgenic controls. RESULTS: Cu accumulates in non-CNS tissues at pre-symptomatic stages in SOD1 tissues. This accumulation represents a potentially pathological feature that cannot solely be explained by the over-expression of mSOD1. As a result of the lack of Cu uptake into the CNS there may be a deficiency of Cu for the over-expressed mutant SOD1 in these tissues. Elevated Cu concentrations in muscle tissue also preceded the onset of symptoms and were found to be pathological and not be the result of SOD1 over-expression. CONCLUSIONS: It is hypothesized that the observed Cu accumulations may represent a pathologic feature of ALS, which may actively contribute to axonal retraction leading to muscular denervation, and possibly significantly contributing to disease pathology. Therefore, it is proposed that the toxic-gain-of-function and dying-back hypotheses to explain the molecular drivers of ALS may not be separate, individual processes; rather our data suggests that they are parallel processes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 48876 MEDLINE  
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[PMID]: 29524627
[Au] Autor:Matschke LA; Rinné S; Snutch TP; Oertel WH; Dolga AM; Decher N
[Ad] Address:Institute for Physiology and Pathophysiology, Vegetative Physiology and Marburg Center for Mind, Brain and Behavior - MCMBB, Philipps-University Marburg, 35037 Marburg, Germany; Clinic for Neurology, Philipps-University Marburg, 35037 Marburg, Germany. Electronic address: lina.matschke@staff.uni-mar
[Ti] Title:Calcium-activated SK potassium channels are key modulators of the pacemaker frequency in locus coeruleus neurons.
[So] Source:Mol Cell Neurosci;, 2018 Mar 07.
[Is] ISSN:1095-9327
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The physiological, intrinsic activity of noradrenergic locus coeruleus (LC) neurons is important for the control of sleep/wakefulness, cognition and autonomous body functions. Dysregulations of the LC-noradrenergic network contribute to the pathogenesis of psychiatric disorders and are key findings in early stages of neurodegenerative diseases. Therefore, identifying ion channels mediating the intrinsic pacemaking mechanism of LC neurons, which is in turn directly coupled to Ca homeostasis and cell survival signaling pathways, can help to foster our understanding of the vulnerability of these neurons in neurodegenerative diseases. Small-conductance Ca -activated K (SK) channels regulate the intrinsic firing patterns in different central neurons and are essential regulators of the intracellular Ca homeostasis. However, the role of SK channels for the intrinsic pacemaking of LC neurons in mice is still unclear. Therefore we performed qPCR expression analysis as well as patch clamp recordings of in vitro brainstem slices, for instance testing SK channel blockers and activators like apamin and NS309, respectively. Although we found a transcriptional expression of SK1, SK2 and SK3 channels, SK2 was the predominantly expressed subunit in mouse LC neurons. Using perforated-patch clamp experiments, we found that SK channels are essential regulators of the intrinsic pacemaking of LC neurons, mediating a large fraction of the afterhyperpolarization (AHP) in these cells. Consistent with previous observations that a concerted action of L- and T-type Cav channels is essential for the pacemaking of LC neurons, we found that SK channel activation, and the respective AHP amplitude, is primarily coupled to Ca influx via these types of Ca channels. Our study identified SK2 channels as drug targets for the tuning of the pacemaker frequency in disorders involving a dysregulation of the LC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 48876 MEDLINE  
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[PMID]: 29511163
[Au] Autor:Delprat B; Maurice T; Delettre C
[Ad] Address:INSERM UMR-S1198, 34095, Montpellier, France. benjamin.delprat@inserm.fr.
[Ti] Title:Wolfram syndrome: MAMs' connection?
[So] Source:Cell Death Dis;9(3):364, 2018 Mar 06.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Wolfram syndrome (WS) is a rare neurodegenerative disease, the main pathological hallmarks of which associate with diabetes, optic atrophy, and deafness. Other symptoms may be identified in some but not all patients. Prognosis is poor, with death occurring around 35 years of age. To date, no treatment is available. WS was first described as a mitochondriopathy. However, the localization of the protein on the endoplasmic reticulum (ER) membrane challenged this hypothesis. ER contacts mitochondria to ensure effective Ca transfer, lipids transfer, and apoptosis within stabilized and functionalized microdomains, termed "mitochondria-associated ER membranes" (MAMs). Two types of WS are characterized so far and Wolfram syndrome type 2 is due to mutation in CISD2, a protein mostly expressed in MAMs. The aim of the present review is to collect evidences showing that WS is indeed a mitochondriopathy, with established MAM dysfunction, and thus share commonalities with several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as metabolic diseases, such as diabetes.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0406-3

  4 / 48876 MEDLINE  
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[PMID]: 29477598
[Au] Autor:Jiang X; Wang X; Tuo M; Ma J; Xie A
[Ad] Address:Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, China.
[Ti] Title:RAGE and its emerging role in the pathogenesis of Parkinson's disease.
[So] Source:Neurosci Lett;672:65-69, 2018 Feb 27.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Receptor for advanced glycation end products (RAGE) is a multiligand receptor belonging to the immunoglobulin superfamily and plays crucial roles in the development of many human diseases such as neurodegenerative diseases, diabetes, cardiovascular diseases, osteoarthritis and cancer. RAGE involves in a number of cell processes such as neuroinflammation, apoptosis, proliferation and autophagy. In CNS, RAGE was primarily expressed in neurons, microglia and vascular endothelial cells. Interacting with ligands, RAGE induces a series of signal transduction cascades and leads to the activation of transcription factor NF-κB as well as increased expression of cytokines like TNF-α, IL-1. Moreover, binding to RAGE can also stimulate the generation of reactive oxygen species (ROS), which is implicated in neuron death. It was reported that RAGE were highly expressed in PD patients when compared to age-matched controls. And RAGE ablation protected nigral dopaminergic neurons against cell death in MPTP treated mice. Here we review this article to elucidate the role of RAGE in PD pathogenesis and highlight the anti-RAGE strategies in the treatment of PD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 48876 MEDLINE  
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[PMID]: 29474873
[Au] Autor:Jensen HLB; Lillenes MS; Rabano A; Günther CC; Riaz T; Kalayou ST; Ulstein ID; Bøhmer T; Tønjum T
[Ad] Address:Department of Microbiology, University of Oslo, Oslo, Norway. Electronic address: h.l.b.jensen@studmed.uio.no.
[Ti] Title:Expression of nucleotide excision repair in Alzheimer's disease is higher in brain tissue than in blood.
[So] Source:Neurosci Lett;672:53-58, 2018 Feb 21.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Age-related changes are increased in patients with Alzheimer's disease (AD), including oxidative stress and DNA damage. We propose that genotoxic stress and DNA repair responses influence neurodegeneration in the pathogenesis of AD. Here, we focus on nucleotide excision repair (NER). Real-time qPCR and mass spectrometry were employed to determine the expression levels of selected NER components. The mRNA levels of the genes encoding the NER proteins RAD23B, RPA1, ERCC1, PCNA and LIG3 as well as the NER-interacting base excision repair protein MPG in blood and brain tissue from four brain regions in patients with AD or mild cognitive impairment and healthy controls (HC), were assessed. NER mRNA levels were significantly higher in brain tissue than in blood. Further, LIG3 mRNA levels in the frontal cortex was higher in AD versus HC, while mRNA levels of MPG and LIG3 in entorhinal cortex and RPA1 in the cerebellum were lower in AD versus HC. In blood, RPA1 and ERCC1 mRNA levels were lower in AD patients than in HC. Alterations in gene expression of NER components between brain regions were associated with AD, connecting DNA repair to AD pathogenesis and suggesting a distinct role for NER in the brain.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  6 / 48876 MEDLINE  
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[PMID]: 29462705
[Au] Autor:Ghasemi M; Mayasi Y; Hannoun A; Eslami SM; Carandang R
[Ad] Address:Department of Neurology, University of Massachusetts Medical School, Worcester, MA 01655, USA. Electronic address: mehdi.ghasemi@umassmemorial.org.
[Ti] Title:Nitric Oxide and Mitochondrial Function in Neurological Diseases.
[So] Source:Neuroscience;376:48-71, 2018 Feb 17.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Mitochondria are key cellular organelles that play crucial roles in the energy production and regulation of cellular metabolism. Accumulating evidence suggests that mitochondrial activity can be modulated by nitric oxide (NO). As a key neurotransmitter in biologic systems, NO mediates the majority of its function through activation of the cyclic guanylyl cyclase (cGC) signaling pathway and S-nitrosylation of a variety of proteins involved in cellular functioning including those involved in mitochondrial biology. Moreover, excess NO or the formation of reactive NO species (RNS), e.g., peroxynitrite (ONOO ), impairs mitochondrial functioning and this, in conjunction with nuclear events, eventually affects neuronal cell metabolism and survival, contributing to the pathogenesis of several neurodegenerative diseases. In this review we highlight the possible mechanisms underlying the noxious effects of excess NO and RNS on mitochondrial function including (i) negative effects on electron transport chain (ETC); (ii) ONOO -mediated alteration in mitochondrial permeability transition; (iii) enhanced mitochondrial fragmentation and autophagy through S-nitrosylation of key proteins involved in this process such as dynamin-related protein 1 (DRP-1) and Parkin/PINK1 (protein phosphatase and tensin homolog-induced kinase 1) complex; (iv) alterations in the mitochondrial metabolic pathways including Krebs cycle, glycolysis, fatty acid metabolism, and urea cycle; and finally (v) mitochondrial ONOO -induced nuclear toxicity and subsequent release of apoptosis-inducing factor (AIF) from mitochondria, causing neuronal cell death. These proposed mechanisms highlight the multidimensional nature of NO and its signaling in the mitochondrial function. Understanding the mechanisms by which NO mediates mitochondrial (dys)function can provide new insights into the treatment of neurodegenerative diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 48876 MEDLINE  
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[PMID]: 29462608
[Au] Autor:Khalil B; Morderer D; Price PL; Liu F; Rossoll W
[Ad] Address:Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224 USA.
[Ti] Title:mRNP assembly, axonal transport, and local translation in neurodegenerative diseases.
[So] Source:Brain Res;, 2018 Feb 17.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The development, maturation, and maintenance of the mammalian nervous system rely on complex spatiotemporal patterns of gene expression. In neurons, this is achieved by the expression of differentially localized isoforms and specific sets of mRNA-binding proteins (mRBPs) that regulate RNA processing, mRNA trafficking, and local protein synthesis at remote sites within dendrites and axons. There is growing evidence that axons contain a specialized transcriptome and are endowed with the machinery that allows them to rapidly alter their local proteome via local translation and protein degradation. This enables axons to quickly respond to changes in their environment during development, and to facilitate axon regeneration and maintenance in adult organisms. Aside from providing autonomy to neuronal processes, local translation allows axons to send retrograde injury signals to the cell soma. In this review, we discuss evidence that disturbances in mRNP transport, granule assembly, axonal localization, and local translation contribute to pathology in various neurodegenerative diseases, including spinal muscular atrophy (SMA), amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  8 / 48876 MEDLINE  
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[PMID]: 29397305
[Au] Autor:Gordon BA; Blazey TM; Su Y; Hari-Raj A; Dincer A; Flores S; Christensen J; McDade E; Wang G; Xiong C; Cairns NJ; Hassenstab J; Marcus DS; Fagan AM; Jack CR; Hornbeck RC; Paumier KL; Ances BM; Berman SB; Brickman AM; Cash DM; Chhatwal JP; Correia S; Förster S; Fox NC; Graff-Radford NR; la Fougère C; Levin J; Masters CL; Rossor MN; Salloway S; Saykin AJ; Schofield PR; Thompson PM; Weiner MM; Holtzman DM; Raichle ME; Morris JC; Bateman RJ; Benzinger TLS
[Ad] Address:Mallinckrodt Institute of Radiology, Washington University, St Louis, MO, USA; Knight Alzheimer's Disease Research Center, Washington University, St Louis, MO, USA; Department of Psychological & Brain Sciences, Washington University, St Louis, MO, USA. Electronic address: bagordon@wustl.edu.
[Ti] Title:Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer's disease: a longitudinal study.
[So] Source:Lancet Neurol;17(3):241-250, 2018 Mar.
[Is] ISSN:1474-4465
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Models of Alzheimer's disease propose a sequence of amyloid ß (Aß) accumulation, hypometabolism, and structural decline that precedes the onset of clinical dementia. These pathological features evolve both temporally and spatially in the brain. In this study, we aimed to characterise where in the brain and when in the course of the disease neuroimaging biomarkers become abnormal. METHODS: Between Jan 1, 2009, and Dec 31, 2015, we analysed data from mutation non-carriers, asymptomatic carriers, and symptomatic carriers from families carrying gene mutations in presenilin 1 (PSEN1), presenilin 2 (PSEN2), or amyloid precursor protein (APP) enrolled in the Dominantly Inherited Alzheimer's Network. We analysed C-Pittsburgh Compound B ( C-PiB) PET, F-Fluorodeoxyglucose ( F-FDG) PET, and structural MRI data using regions of interest to assess change throughout the brain. We estimated rates of biomarker change as a function of estimated years to symptom onset at baseline using linear mixed-effects models and determined the earliest point at which biomarker trajectories differed between mutation carriers and non-carriers. This study is registered at ClinicalTrials.gov (number NCT00869817) FINDINGS: C-PiB PET was available for 346 individuals (162 with longitudinal imaging), F-FDG PET was available for 352 individuals (175 with longitudinal imaging), and MRI data were available for 377 individuals (201 with longitudinal imaging). We found a sequence to pathological changes, with rates of Aß deposition in mutation carriers being significantly different from those in non-carriers first (across regions that showed a significant difference, at a mean of 18·9 years [SD 3·3] before expected onset), followed by hypometabolism (14·1 years [5·1] before expected onset), and lastly structural decline (4·7 years [4·2] before expected onset). This biomarker ordering was preserved in most, but not all, regions. The temporal emergence within a biomarker varied across the brain, with the precuneus being the first cortical region for each method to show divergence between groups (22·2 years before expected onset for Aß accumulation, 18·8 years before expected onset for hypometabolism, and 13·0 years before expected onset for cortical thinning). INTERPRETATION: Mutation carriers had elevations in Aß deposition, reduced glucose metabolism, and cortical thinning compared with non-carriers which preceded the expected onset of dementia. Accrual of these pathologies varied throughout the brain, suggesting differential regional and temporal vulnerabilities to Aß, metabolic decline, and structural atrophy, which should be taken into account when using biomarkers in a clinical setting as well as designing and evaluating clinical trials. FUNDING: US National Institutes of Health, the German Center for Neurodegenerative Diseases, and the Medical Research Council Dementias Platform UK.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[Cl] Clinical Trial:ClinicalTrial
[St] Status:In-Data-Review

  9 / 48876 MEDLINE  
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[PMID]: 29324989
[Au] Autor:Bereczki E; Branca RM; Francis PT; Pereira JB; Baek JH; Hortobágyi T; Winblad B; Ballard C; Lehtiö J; Aarsland D
[Ad] Address:Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, Novum, Stockholm, Sweden.
[Ti] Title:Synaptic markers of cognitive decline in neurodegenerative diseases: a proteomic approach.
[So] Source:Brain;141(2):582-595, 2018 Feb 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:See Attems and Jellinger (doi:10.1093/brain/awx360) for a scientific commentary on this article.Cognitive changes occurring throughout the pathogenesis of neurodegenerative diseases are directly linked to synaptic loss. We used in-depth proteomics to compare 32 post-mortem human brains in the prefrontal cortex of prospectively followed patients with Alzheimer's disease, Parkinson's disease with dementia, dementia with Lewy bodies and older adults without dementia. In total, we identified 10 325 proteins, 851 of which were synaptic proteins. Levels of 25 synaptic proteins were significantly altered in the various dementia groups. Significant loss of SNAP47, GAP43, SYBU (syntabulin), LRFN2, SV2C, SYT2 (synaptotagmin 2), GRIA3 and GRIA4 were further validated on a larger cohort comprised of 92 brain samples using ELISA or western blot. Cognitive impairment before death and rate of cognitive decline significantly correlated with loss of SNAP47, SYBU, LRFN2, SV2C and GRIA3 proteins. Besides differentiating Parkinson's disease dementia, dementia with Lewy bodies, and Alzheimer's disease from controls with high sensitivity and specificity, synaptic proteins also reliably discriminated Parkinson's disease dementia from Alzheimer's disease patients. Our results suggest that these particular synaptic proteins have an important predictive and discriminative molecular fingerprint in neurodegenerative diseases and could be a potential target for early disease intervention.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx352

  10 / 48876 MEDLINE  
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[PMID]: 29282337
[Au] Autor:La Joie R; Bejanin A; Fagan AM; Ayakta N; Baker SL; Bourakova V; Boxer AL; Cha J; Karydas A; Jerome G; Maass A; Mensing A; Miller ZA; O'Neil JP; Pham J; Rosen HJ; Tsai R; Visani AV; Miller BL; Jagust WJ; Rabinovici GD
[Ad] Address:From the Memory and Aging Center (R.L.J., A.B., N.A., V.B., A.L.B., J.C., A.K., A.M., Z.A.M., J.P., H.J.R., R.T., A.V., B.L.M., G.D.R.), University of California San Francisco; Knight Alzheimer's Disease Research Center (A.M.F., G.J.), Department of Neurology (A.M.F., G.J.), and The Hope Center for
[Ti] Title:Associations between [ F]AV1451 tau PET and CSF measures of tau pathology in a clinical sample.
[So] Source:Neurology;90(4):e282-e290, 2018 Jan 23.
[Is] ISSN:1526-632X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To assess the relationships between fluid and imaging biomarkers of tau pathology and compare their diagnostic utility in a clinically heterogeneous sample. METHODS: Fifty-three patients (28 with clinical Alzheimer disease [AD] and 25 with non-AD clinical neurodegenerative diagnoses) underwent ß-amyloid (Aß) and tau ([ F]AV1451) PET and lumbar puncture. CSF biomarkers (Aß , total tau [t-tau], and phosphorylated tau [p-tau]) were measured by multianalyte immunoassay (AlzBio3). Receiver operator characteristic analyses were performed to compare discrimination of Aß-positive AD from non-AD conditions across biomarkers. Correlations between CSF biomarkers and PET standardized uptake value ratios (SUVR) were assessed using skipped Pearson correlation coefficients. Voxelwise analyses were run to assess regional CSF-PET associations. RESULTS: [ F]AV1451-PET cortical SUVR and p-tau showed excellent discrimination between Aß-positive AD and non-AD conditions (area under the curve 0.92-0.94; ≤0.83 for other CSF measures), and reached 83% classification agreement. In the full sample, cortical [ F]AV1451 was associated with all CSF biomarkers, most strongly with p-tau ( = 0.75 vs 0.57 for t-tau and -0.49 for Aß ). When restricted to Aß-positive patients with AD, [ F]AV1451 SUVR correlated modestly with p-tau and t-tau (both = 0.46) but not Aß ( = 0.02). On voxelwise analysis, [ F]AV1451 correlated with CSF p-tau in temporoparietal cortices and with t-tau in medial prefrontal regions. Within AD, Mini-Mental State Examination scores were associated with [ F]AV1451-PET, but not CSF biomarkers. CONCLUSION: [ F]AV1451-PET and CSF p-tau had comparable value for differential diagnosis. Correlations were robust in a heterogeneous clinical group but attenuated (although significant) in AD, suggesting that fluid and imaging biomarkers capture different aspects of tau pathology. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that, in a clinical sample of patients with a variety of suspected neurodegenerative diseases, both CSF p-tau and [ F]AV1451 distinguish AD from non-AD conditions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1212/WNL.0000000000004860


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