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Effect of Alzheimer Familial Chromosomal Mutations on the Amyloid Fibril Interaction with Different PET Tracers: Insight from Molecular Modeling Studies.

https://arctichealth.org/en/permalink/ahliterature285616
Source
ACS Chem Neurosci. 2017 Oct 03;
Publication Type
Article
Date
Oct-03-2017
Author
Kanagasabai Balamurugan
Natarajan Arul Murugan
Bengt Långström
Agneta Nordberg
Hans Ågren
Source
ACS Chem Neurosci. 2017 Oct 03;
Date
Oct-03-2017
Language
English
Publication Type
Article
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disorder. Along with an increasing number of elderly worldwide, it poses a great challenge for the society and health care. Although sporadic AD is the common form of AD, 2-3% of the AD cases are expected to be due to mutations in the ? region of the amyloid precursor protein, which is referred to as autosomal dominant AD (ADAD). These mutations may cause changes in the secondary structure of the amyloid ? fibrils and may alter the fibrillization rate leading to changes in the disease development and could also affect the binding to tracers used in diagnosis. In particular, from some recent clinical studies using PET tracers for detection of fibrillar amyloids, it is evident that in ADAD patients with Arctic mutation no amyloid plaque binding can be detected with the (11)C-Pittsburgh Compound B ((11)C-PIB). However, for in vitro conditions, significant binding of (3)H-PIB has been reported for the amyloid fibrils carrying the Arctic mutation. The aim of the present study is to investigate if there is any mutation specific binding of commonly used amyloid tracers, namely, florbetaben, florbetapir, FPIB, AZD4694, and AZD2184, by means of molecular modeling techniques. Other than Arctic, ADAD mutations, such as the Dutch, Italian, Iowa, and Flemish mutations, are considered in this study. We report that all tracers except florbetapir show reduced binding affinity toward amyloid ? fibrils with the Arctic mutation when compared to the native type. Moreover, florbetapir is the only tracer that binds to all mutants with increased affinity when compared to the native fibril. The results obtained from these studies could increase the understanding of the structural changes caused by mutation and concomitant changes in the interaction pattern of the PET tracers with the mutated variants, which in turn can be useful in selecting the appropriate tracers for the purpose of diagnosis as well as for designing new tracers with desirable properties.
PubMed ID
28898051 View in PubMed
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Improving the diagnosis and management of neuroendocrine tumors: utilizing new advances in biomarker and molecular imaging science.

https://arctichealth.org/en/permalink/ahliterature115978
Source
Neuroendocrinology. 2013;98(1):16-30
Publication Type
Conference/Meeting Material
Article
Date
2013
Author
Valeria Giandomenico
Irvin M Modlin
Fredrik Pontén
Mats Nilsson
Ulf Landegren
Jonas Bergqvist
Mohid S Khan
Robert P Millar
Bengt Långström
Jürgen Borlak
Barbro Eriksson
Bengt Nielsen
Lars Baltzer
John C Waterton
Håkan Ahlström
Kjell Öberg
Author Affiliation
Department of Medical Sciences, Endocrine Oncology, University Hospital, Uppsala, Sweden.
Source
Neuroendocrinology. 2013;98(1):16-30
Date
2013
Language
English
Publication Type
Conference/Meeting Material
Article
Keywords
Disease Management
Humans
Molecular Imaging - standards - trends
Neuroendocrine Tumors - diagnosis - metabolism - therapy
Sweden
Tumor Markers, Biological - metabolism
Abstract
Neuroendocrine tumors (NET) are malignant solid tumors that arise in hormone-secreting tissue of the diffuse neuroendocrine system or endocrine glands. Although traditionally understood to be a rare disease, the incidence and prevalence of NET have increased greatly in the past 3 decades. However, during this time, progress in diagnosis and outcome of NET has generally been modest. In order to achieve improved outcome in NET, a better understanding of NET biology combined with more reliable serum markers and better techniques to identify tumor localization and small lesions are needed. Although some NET biomarkers exist, sensitive and specific markers that predict tumor growth and behavior are generally lacking. In addition, the integration of new molecular imaging technologies in patient diagnosis and follow-up has the potential to enhance care. To discuss developments and issues required to improve diagnostics and management of NET patients, with specific focus on the latest advances in molecular imaging and biomarker science, 17 global leaders in the fields of NET, molecular imaging and biomarker technology gathered to participate in a 2-day meeting hosted by Prof. Kjell Öberg at the University of Uppsala in Sweden. During this time, findings were presented regarding methods with potential prognostic and treatment applications in NET or other types of cancers. This paper describes the symposium presentations and resulting discussions.
PubMed ID
23446227 View in PubMed
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Low PiB PET retention in presence of pathologic CSF biomarkers in Arctic APP mutation carriers.

https://arctichealth.org/en/permalink/ahliterature123422
Source
Neurology. 2012 Jul 17;79(3):229-36
Publication Type
Article
Date
Jul-17-2012
Author
Michael Schöll
Anders Wall
Steinunn Thordardottir
Daniel Ferreira
Nenad Bogdanovic
Bengt Långström
Ove Almkvist
Caroline Graff
Agneta Nordberg
Author Affiliation
Department of Neurobiology, Care Sciences, and Society, Karolinska Institutet, Stockholm, Sweden.
Source
Neurology. 2012 Jul 17;79(3):229-36
Date
Jul-17-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Alzheimer Disease - cerebrospinal fluid - genetics - radionuclide imaging
Amyloid beta-Peptides - cerebrospinal fluid - genetics
Aniline Compounds - diagnostic use
Atrophy
Biological Markers - cerebrospinal fluid
Carbon Radioisotopes - diagnostic use
Cognition - physiology
Female
Fluorodeoxyglucose F18 - diagnostic use
Humans
Image Processing, Computer-Assisted
Magnetic Resonance Imaging
Male
Middle Aged
Mutation - genetics
Neuropsychological Tests
Peptide Fragments - cerebrospinal fluid
Presenilin-1 - genetics
Radiopharmaceuticals - diagnostic use
Thiazoles - diagnostic use
tau Proteins - cerebrospinal fluid
Abstract
To investigate the particular pathology of the Arctic APP (APParc) early-onset familial Alzheimer disease (eoFAD) mutation for the first time in vivo with PET in comparison with other eoFAD mutations and sporadic Alzheimer disease (sAD).
We examined 2 APParc mutation carriers together with 5 noncarrier siblings cross-sectionally with (11)C-labeled Pittsburgh compound B (PiB) and (18)F-fluorodeoxyglucose (FDG) PET, as well as MRI, CSF biomarkers, and neuropsychological tests. Likewise, we examined 7 patients with sAD, 1 carrier of a presenilin 1 (PSEN1) mutation, 1 carrier of the Swedish APP (APPswe) mutation, and 7 healthy controls (HCs).
Cortical PiB retention was very low in the APParc mutation carriers while cerebral glucose metabolism and CSF levels of A?(1-42), total and phosphorylated tau were clearly pathologic. This was in contrast to the PSEN1 and APPswe mutation carriers revealing high PiB retention in the cortex and the striatum in combination with abnormal glucose metabolism and CSF biomarkers, and the patients with sAD who showed typically high cortical PiB retention and pathologic CSF levels as well as decreased glucose metabolism when compared with HCs.
The lack of fibrillar ?-amyloid (A?) as visualized by PiB PET in APParc mutation carriers suggests, given the reduced glucose metabolism and levels of A?(1-42) in CSF, that other forms of A? such as oligomers and protofibrils are important for the pathologic processes leading to clinical Alzheimer disease.
Notes
Comment In: Neurology. 2012 Jul 17;79(3):206-722700807
PubMed ID
22700814 View in PubMed
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