Publications by authors named "Allan K Hansen"

Background: Until recently, quantitation of the net influx of 2-[F]fluorodeoxyglucose (FDG) to brain (K) and the cerebrometabolic rate for glucose (CMR) required serial arterial blood sampling in conjunction with dynamic positron emission tomography (PET) recordings. Recent technical innovations enable the identification of an image-derived input function (IDIF) from vascular structures, but are frequently still encumbered by the need for interrupted sequences or prolonged recordings that are seldom available outside of a research setting. In this study, we tested simplified methods for quantitation of FDG-K by linear graphic analysis relative to the descending aorta IDIF in oncology patients examined using a Biograph Vision 600 PET/CT with continuous bed motion (Aarhus) or using a recently installed Biograph Vision Quadra long-axial field-of-view (FOV) scanner (Bern).

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Dementia with Lewy bodies is characterized by a high burden of autonomic dysfunction and Lewy pathology in peripheral organs and components of the sympathetic and parasympathetic nervous system. Parasympathetic terminals may be quantified with 18F-fluoroetoxybenzovesamicol, a PET tracer that binds to the vesicular acetylcholine transporter in cholinergic presynaptic terminals. Parasympathetic imaging may be useful for diagnostics, improving our understanding of autonomic dysfunction and for clarifying the spatiotemporal relationship of neuronal degeneration in prodromal disease.

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Cholinergic changes play a fundamental role in the natural history of dementia with Lewy bodies and Lewy body disease in general. Despite important achievements in the field of cholinergic research, significant challenges remain. We conducted a study with four main objectives: (i) to examine the integrity of cholinergic terminals in newly diagnosed dementia with Lewy bodies; (ii) to disentangle the cholinergic contribution to dementia by comparing cholinergic changes in Lewy body patients with and without dementia; (iii) to investigate the in vivo relationship between cholinergic terminal loss and atrophy of cholinergic cell clusters in the basal forebrain at different stages of Lewy body disease; and (iv) to test whether any asymmetrical degeneration in cholinergic terminals would correlate with motor dysfunction and hypometabolism.

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Background: The α-syn Origin site and Connectome model (SOC) proposes that α-synucleinopathies can be divided into two categories: the asymmetrical brain-first, and more symmetrical body-first Lewy body disease. We have hypothesized that most patients with dementia with Lewy bodies (DLB) belong to the body-first subtype, whereas patients with Parkinson's disease (PD) more often belong to the brain-first subtype.

Objective: To compare asymmetry of striatal dopaminergic dysfunction in DLB and PD patients using [18F]-FE-PE2I positron emission tomography (PET).

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Article Synopsis
  • Patients with Lewy body diseases show varying levels of brain metabolism reduction, which may be linked to synaptic degeneration, though the exact reasons for this decline remain unclear.
  • The study aimed to explore if local synaptic loss in the cortex correlates with decreased brain metabolism by using PET scans to measure both glucose metabolism and synaptic density.
  • Results indicated that while both synaptic density and glucose consumption were reduced in patients, the reduction in glucose uptake was greater than the decline in synaptic density, suggesting other factors contribute to hypometabolism in Lewy body disorders.
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  • Isolated rapid eye movement sleep behavior disorder (iRBD) involves abnormal movements and vocalizations during REM sleep, serving as an early indicator of neurodegenerative diseases like Parkinson's and Lewy body dementia.
  • This study analyzed data from 171 iRBD patients and 238 healthy controls using advanced imaging techniques to understand the genetic and structural brain changes associated with iRBD.
  • Key findings highlighted significant alterations in gene expression related to mitochondrial function and brain atrophy, suggesting possible underlying mechanisms for these neurodegenerative processes.
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Introduction: [F]fluoroetoxybenzovesamicol ([F]FEOBV) is a positron emission topography (PET) tracer for the vesicular acetylcholine transporter (VAChT), a protein located predominantly in synaptic vesicles in cholinergic nerve terminals. We aimed to use [F]FEOBV PET to study the cholinergic topography of the healthy human brain.

Materials And Methods: [F]FEOBV PET brain data volumes of healthy elderly humans were normalized to standard space and intensity-normalized to the white matter.

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Background: Cholinergic degeneration is strongly associated with cognitive decline in patients with Parkinson's disease (PD) but may also cause motor symptoms and olfactory dysfunction. Regional differences are striking and may reflect different PD related symptoms and disease progression patterns.

Objective: To map and quantify the regional cerebral cholinergic alterations in non-demented PD patients.

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Background: Although sleep disturbances are highly prevalent in patients with Parkinson's disease, sleep macroarchitecture metrics show only minor changes.

Objective: To assess alterations of the cyclic alternating pattern (CAP) as a critical feature of sleep microarchitecture in patients with prodromal, recent, and established Parkinson's disease.

Methods: We evaluated overnight polysomnography for classic sleep macroarchitecture and CAP metrics in 68 patients at various disease stages and compared results to 22 age- and sex-matched controls.

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Background: The average human lifespan has increased dramatically over the past century. However, molecular and physiological alterations of the healthy brain during aging remain incompletely understood. Generalized synaptic restructuring may contribute to healthy aging and the reduced metabolism observed in the aged brain.

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Background: Dynamic whole-body (D-WB) FDG PET/CT is a recently developed technique that allows direct reconstruction of multiparametric images of metabolic rate of FDG uptake (MR) and "free" FDG (DV). Multiparametric images have a markedly different appearance than the conventional SUV images obtained by static PET imaging, and normal values of MR and DV in frequently used reference tissues and organs are lacking. The aim of this study was therefore to: (1) provide an overview of normal MR and DV values and range of variation in organs and tissues; (2) analyse organ time-activity curves (TACs); (3) validate the accuracy of directly reconstructed MR tissue values versus manually calculated K (and MR) values; and (4) explore correlations between demographics, blood glucose levels and MR values.

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A 76-year-old man with newly diagnosed high-risk prostate cancer was referred for primary staging with F-18-PSMA-1007 PET/CT. The PET/CT scan showed no lymph node or bone metastases, only localized disease within the prostate gland. Additionally, the F-18-PSMA PET/CT scan showed a PSMA-positive lesion correlating to a polyp located in the body of the stomach on the greater curvature.

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Ménière's disease (MD) is a chronic peripheral vestibular disorder with recurrent episodes of vertigo accompanied by fluctuating hearing loss, tinnitus and aural fullness in the affected ear. There are several unanswered fundamental questions regarding MD, one of these being cortical activity during a MD attack. However, it is not possible to plan an investigation in an episodic disease as MD.

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Previous studies have reported substantial involvement of the noradrenergic system in Parkinson's disease. Neuromelanin-sensitive MRI sequences and PET tracers have become available to visualize the cell bodies in the locus coeruleus and the density of noradrenergic terminal transporters. Combining these methods, we investigated the relationship of neurodegeneration in these distinct compartments in Parkinson's disease.

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Background: Patients with Parkinson's disease (PD) often develop dementia, but the underlying substrate is incompletely understood. Generalized synaptic degeneration may contribute to dysfunction and cognitive decline in Lewy body dementias, but in vivo evidence is lacking.

Objective: The objective of this study was to assess the density of synapses in non-demented PD (nPD) subjects (N = 21), patients with PD-dementia or Dementia with Lewy bodies (DLB) (N = 13), and age-matched healthy controls (N = 15).

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Study Objectives: Parkinson's disease (PD) commonly involves degeneration of sleep-wake regulating brainstem nuclei; likewise, sleep-wake disturbances are highly prevalent in PD patients. As polysomnography macroparameters typically show only minor changes in PD, we investigated sleep microstructure, particularly cyclic alternating pattern (CAP), and its relation to alterations of the noradrenergic system in these patients.

Methods: We analyzed 27 PD patients and 13 healthy control (HC) subjects who underwent overnight polysomnography and 11C-MeNER positron emission tomography for evaluation of noradrenaline transporter density.

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Article Synopsis
  • The study investigates norepinephrine transporter (NART) binding in the sensorimotor cortex of patients with idiopathic rapid-eye-movement sleep behavior disorder (iRBD) and Parkinson's disease (PD), suggesting a link to motor dysfunction.
  • iRBD and PD patients showed significant reductions in NART binding compared to healthy controls, indicating altered noradrenergic neurotransmission.
  • A correlation was found between thalamic C-MeNER binding and putaminal F-DOPA uptake in iRBD patients, suggesting parallel degeneration of neurotransmitter systems in this early stage of PD.
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Background: The aim of this longitudinal study was to assess with positron emission tomography (PET) the relationship between levels of inflammation and the loads of aggregated β-amyloid and tau at baseline and again after 2 years in prodromal Alzheimer's disease.

Methods: Forty-three subjects with mild cognitive impairment (MCI) had serial C-PK11195 PET over 2 years to measure inflammation changes, and C-PiB PET to determine β-amyloid fibril load; 22 also had serial F-Flortaucipir PET to determine tau tangle load. Cortical surface statistical mapping was used to localise areas showing significant changes in tracer binding over time and to interrogate correlations between tracer binding of the tracers at baseline and after 2 years.

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The cortical metabolic activity in patients with Menière's disease has not been investigated. The aim of this study was to investigate the F-FDG cerebral uptake in Menière's patients compared to healthy controls. Eight patients with right-sided Menière's disease and fourteen healthy controls underwent a video head impulse test (vHIT), test of utricular function with ocular vestibular evoked myogenic potentials (oVEMP) and three F-FDG-based PET examinations of the brain.

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Background: Flortaucipir PET, a marker of tau tangles, has shown lower than expected cortical uptake in Parkinson's disease (PD), than would be predicted from neuropathologic estimates of Alzheimer's disease co-pathology. Instead, the most characteristic finding of flortaucipir imaging in PD is decreased uptake in the substantia nigra, reflecting reduction in its "off-target" binding to neuromelanin. We have previously reported these observations in cross-sectional studies.

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The existence of a human primary vestibular cortex is still debated. Current knowledge mainly derives from functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) acquisitions during artificial vestibular stimulation. This may be problematic as artificial vestibular stimulation entails coactivation of other sensory receptors.

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Background: Donepezil may have cardioprotective properties, but the mechanism is unclear. Using positron-emission tomography (PET), we explored C-donepezil uptake in the heart of humans in relation to age. The results are discussed in the context of the cardioprotective property of donepezil.

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder. AD pathology is characterized by abnormal aggregation of the proteins amyloid- (A) and hyperphosphorylated tau. No effective disease modifying therapies are currently available.

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