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Multicentre Studies
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Terez Sera, Ronald Boellaard, Andres Kaalep, Michael Ljungberg
Multicentre trials involving nuclear medicine imaging have been performed for many years, however, using Single Photon Emission Computed Tomography (SPECT) scanners little data have so far been reported. In 2006, a group of imaging centres from throughout Europe came together under the auspices of EARL to form a brain imaging network of excellence. The first task of this group was to produce a normal control database of 123I-FP-CIT SPECT studies in a multicentre setting [30]. For this project the group used the acronym ENCDAT (European Normal Control Database of DaTSCAN). 123I-FP-CIT (DaTSCAN) is a radiotracer for the dopamine transporter and has been proven to be a useful tool for neurologists, movement disorder specialists, and geriatricians in the diagnosis of Parkinson’s disease, Lewy Body Dementia, and for differentiating such patients from those without loss of dopamine transporters [31–34].
Neurocelebrities in Film
Published in Eelco F. M. Wijdicks, Neurocinema—The Sequel, 2022
A more recent documentary showed another type of dementia. Robin’s Wish (2020) featured Robin Williams and was directed by Tyler Norwood (Figure 7.7). What was his wish—in his own words, to reboot his brain? Robin’s Wish is based on experiences gathered from secondary sources and attempts to show how Robin Williams’s brain could have been working—and, in this interpretation, it is a horror-freak show. Scenes have the camera snooping through empty hallways, snaking around corners, going in and out of focus, and showing tilted images (and all set to minor-key spooky music). The filmmaker employs these tropes to show the problems Williams may have endured.34 The documentary hypothesizes that his diagnosis was missed and that he was treated for Parkinson’s disease rather than Lewy body disease. The documentary has little to say about his use of antidopaminergic drugs, which could have exacerbated his symptoms. Lewy bodies are aggregations of misfolded proteins in the cell, formed when the protein degradation system of the cell is overwhelmed and thought to be responsible for 10% to 15% of dementia cases. People with Lewy body disease experience anxiety, memory loss, hallucinations, and insomnia, and these symptoms are generally accompanied or soon followed by Parkinson’s symptoms. Robin Williams knew something was not right, but nobody could pin it down.
The Aging of the Neuronal Cytoskeleton
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
P. Klosen, Ph. van den Bosch de Aguilar
The Lewy body is the hallmark lesion of Parkinson’s disease. Again, as for the Alzheimer neurofibrillary tangles, Lewy bodies can also be found in old patients without neurological disturbances, although in smaller numbers than in neurological diseases. The Lewy body is composed of densely packed 8- to 10-nm filaments which, at the center of the inclusion, often form a homogeneous granular mass.
Dementia with Lewy bodies: emerging drug targets and therapeutics
Published in Expert Opinion on Investigational Drugs, 2021
Evans D. Pope, Laura Cordes, Jiong Shi, Zoltan Mari, Boris Decourt, Marwan Noel Sabbagh
Dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD) are neurological diseases that share in common α-synuclein (α-syn) pathology that accumulates into Lewy Body pathology, characterized by the toxic accumulation of α-syn protein inside neural cells. Accumulation in α-syn seen in synucleinopathies includes Parkinson’s disease (PD), DLB and multiple system atrophy (MSA). α-syn contributes to the fibrilization of β-amyloid and tau, two pathological hallmarks of AD [1,2]. Patients with DLB have more neuropsychiatric symptoms such as dementia-related psychosis (hallucinations and delusions) [3]. A 2020 study by Smirnov et al. demonstrated that both DLB and PDD patients experienced more severe impairment and a more rapid decline in visuospatial function than AD patients. Patients with PDD demonstrated higher impairment and a more rapid decline in executive functions than patients with DLB or AD. Patients with DLB also demonstrated a more rapid clinical decline than patients with AD, who, in reverse, demonstrated higher memory impairment than patients with DLB. Importantly, the rate of decline was similar for all three groups [4]. DLB patients had more fluctuations, hallucinations, and excessive daytime sleepiness [5].
Therapeutic approaches to cholinergic deficiency in Lewy body diseases
Published in Expert Review of Neurotherapeutics, 2020
Matthew J. Barrett, Leslie J. Cloud, Harsh Shah, Kathryn L. Holloway
Lewy body diseases are neurodegenerative diseases characterized by the presence of intraneuronal Lewy bodies and Lewy neurites. The primary constituent of Lewy bodies is α-synuclein, and thus, Lewy body diseases are also considered α-synucleinopathies along with multiple system atrophy (MSA). The primary Lewy body diseases are Parkinson’s disease (PD), Parkinson’s disease dementia (PDD), and dementia with Lewy bodies (DLB). In PD, an intermediate stage of mild cognitive impairment (PD-MCI) was defined to indicate those who have ‘cognitive decline that is not normal for age but with essentially normal functional activities’ [1]. There are efforts underway to define a diagnostic category for individuals with MCI who do not meet clinical criteria for PD and who are predicted to progress to DLB based on their cognitive profile and the presence of one or more core clinical criteria or indicative biomarkers of DLB [2]. Lastly, evidence has emerged that idiopathic REM sleep behavior disorder (RBD) represents a Lewy body disease in most cases, as most individuals with RBD ultimately develop PD or DLB. The exception to this is the small proportion who are later diagnosed with MSA [3]. It is important to recognize that RBD may be secondary to medications or other sleep disorders. RBD may result from antidepressant or antipsychotic use [4], but at least in the case of antidepressants, emergence of RBD may reflect a susceptibility to developing a Lewy body disease [5].
Pharmacological management of dementia with Lewy bodies with a focus on zonisamide for treating parkinsonism
Published in Expert Opinion on Pharmacotherapy, 2021
Francesco Panza, Madia Lozupone, Mark Watling, Bruno P. Imbimbo
The most recent DLB clinical diagnostic criteria distinguish clearly between clinical features and diagnostic biomarkers [3], although direct biomarker evidence of Lewy body (LB)-related pathology is not yet available to aid clinical diagnosis. However, several useful indirect methods exist including DLB biomarkers that may be indicative or only supportive. Indicative biomarkers for DLB include reduced dopamine transporter (DAT) uptake in basal ganglia demonstrated by single-photon emission computed tomography (SPECT) or positron emission tomography (PET) imaging [11], reduced uptake on metaiodobenzylguanidine (MIBG) myocardial scintigraphy [12], and polysomnographic confirmation of REM sleep without atonia [13].