White matter hyperintensities on MRI in dementia with Lewy bodies, Parkinson's disease with dementia, and Alzheimer's disease

Joki, Hideto; Higashiyama, Yuichi; Nakae, Yoshiharu; Kugimoto, Chiharu; Doi, Hiroshi; Kimura, Kensuke; Kishida, Hitaru; Ueda, Naohisa; Nakano, Tatsu; Takahashi, Tatsuya; Koyano, Shigeru; Takeuchi, Hideyuki; Tanaka, Fumiaki

doi:10.1016/j.jns.2017.12.018

Cited by 49 publications

(60 citation statements)

References 41 publications

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“…White matter involvement in PD is limited, whereas white matter involvement in DLB is variable, mainly affecting the posterior lobes, and often linked with associated Alzheimer's disease (AD) pathology (Bohnen and Albin, 2011;Nedelska et al, 2015;Firbank et al, 2016;Joki et al, 2018). Decreased size of oligodendroglial nuclei has been described in LBD independently of the concomitant AD pathology (Gagyi et al, 2012).…”

Section: Lewy Body Diseasesmentioning

confidence: 99%

“…In addition to these basic alterations, AD exhibits a compendium of biological alterations which modify many molecular pathways and variegated functions (Ferrer, 2012;Braak and Del Tredici, 2015). Reduced size of the white matter, white matter hyperlucencies and myelin pallor are common abnormalities in AD (Barber et al, 1999;Bartzokis et al, 2003;Gouw et al, 2008;Holland et al, 2008;Radanovic et al, 2013;Amlien and Fjell, 2014;Firbank et al, 2016;Joki et al, 2018). Changes in white matter are parallel but do not correlate with β-amyloid deposition (Roseborough et al, 2017), and, importantly, they are recognized at early stages of the disease (Hoy et al, 2017).…”

Section: Alzheimer's Diseasementioning

confidence: 99%

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Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Ferrer

2018

Progress in Neurobiology

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Oligodendrocytes are in contact with neurons, wrap axons with a myelin sheath that protects their structural integrity, and facilitate nerve conduction. Oligodendrocytes also form a syncytium with astrocytes which interacts with neurons, promoting reciprocal survival mediated by activity and by molecules involved in energy metabolism and trophism. Therefore, oligodendrocytes are key elements in the normal functioning of the central nervous system. Oligodendrocytes are affected following different insults to the central nervous system including ischemia, traumatism, and inflammation. The term oligodendrogliopathy highlights the prominent role of altered oligodendrocytes in the pathogenesis of certain neurological diseases, not only in demyelinating diseases and most leukodystrophies, but also in aging and age-related neurodegenerative diseases with abnormal protein aggregates. Most of these diseases are characterized by the presence of abnormal protein deposits, forming characteristic and specific inclusions in neurons and astrocytes but also in oligodendrocytes, thus signaling their involvement in the disease. Emerging evidence suggests that such deposits in oligodendrocytes are not mere bystanders but rather are associated with functional alterations. Moreover, operative modifications in oligodendrocytes are also detected in the absence of oligodendroglial inclusions in certain diseases. The present review focuses first on general aspects of oligodendrocytes and precursors, and their development and functions, and then introduces and updates alterations and dysfunction of oligodendrocytes in selected neurodegenerative diseases with abnormal protein aggregates such as multiple system atrophy, Lewy body diseases, tauopathies, Alzheimer's disease, amyotrophic lateral sclerosis, frontotemporal lobar degeneration with TDP-43 inclusions (TDP-43 proteinopathies), and Creutzfeldt-Jakob´s disease as a prototypical human prionopathy.

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Section: Lewy Body Diseasesmentioning

confidence: 99%

Section: Alzheimer's Diseasementioning

confidence: 99%

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Ferrer

2018

Progress in Neurobiology

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“…The underlying pathology of the WMH signal is heterogeneous and may vary depending on the image intensity [45]. In [40], ADrelated pathology was examined among patients with DLB, PDD, and non-demented PD by associating the WMH severity and medial temporal lobe atrophy. Each subject underwent one or more cognitive evaluations, such as the revised Hasegawa's dementia scale (HDS-R) and MMSE.…”

Section: A Mri Modalitiesmentioning

confidence: 99%

Neuroimaging and Machine Learning for Dementia Diagnosis: Recent Advancements and Future Prospects

Ahmed

Zhang

Feng

et al. 2019

IEEE Rev. Biomed. Eng.

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Dementia, a chronic and progressive cognitive declination of brain function due to disease or impairment, is becoming more prevalent due to the aging population. A major challenge in dementia is achieving the accurate and timely diagnosis. In recent years, neuroimaging with computer-aided algorithms have made remarkable advances in addressing this challenge. Much of the success of these approaches can be attributed to the application of machine learning and deep learning techniques for neuroimaging. In this review paper, we present a comprehensive survey of automated diagnostic approaches for dementia using medical image analysis and machine learning algorithms published in the previous five years (2013-2018). Based on the rigorous review of the existing works, we have found that while most of the studies focused on Alzheimer's disease have demonstrated reasonable performance, the identification of other types of dementia remains a major challenge. Hybrid imaging analysis through deep learning approaches may hold promises for early diagnosis of these other types of dementia, and warrant further investigation in the future. The main contributions of this review paper are as follows: 1. Based on the detailed analysis of the existing literature, this paper discusses the most recent neuroimaging procedures for dementia diagnosis, and 2. It systematically explains the machine learning techniques and, in particular, deep learning approaches for early detection of dementia.

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“…There is similar atrophy of striopallidum but more extensive atrophy of thalamus in DLB. The latter may be a marker of disease severity indicating rapid decline [41], while evaluation of white matter hypointensities and MTL atrophy may indicate progression of AD-related pathology in DLB and perhaps can distinguish DLB from PDD [42,43].…”

Section: Pathophysiology Of Cognitive Impairmentmentioning

confidence: 99%

“…Despite validitated criteria for DLB and PDD [5,13,141], in almost 50% of the cases, the clinical diagnosis is incorrect [142,143], whereas the specificity was below 60% [144]. The sex ratio in DLB is balanced between AD and PDD and, thus, also suggests that DLB is a distinct disease with characteristics intermediate between AD and PD [145], while recent MRI findings indicate that DLB is more similar to AD than to PDD [146].…”

Section: Conclusion and Future Outlookmentioning

confidence: 99%

Dementia with Lewy Bodies and Parkinson's Disease-Dementia: Current Perspectives

A¹

2018

Int J Neurol Neurother

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Dementia with Lewy bodies (DLB) and Parkinson's disease-dementia (PDD) are two closely related major neurocognitive disorders with Lewy bodies of unknown etiology, showing notable overlap in their clinical presentation, pathological features, biochemistry, and genetic risk factors. According to international consensus, their diagnosis is based on an arbitrary distinction between the time of onset of motor and cognitive symptoms: dementia preceding parkinsonism in DLB, while it develops after onset of parkinsonism in PDD (the one-year rule). Clinically, both syndromes show cognitive impairment with severe deficits in executive function, visuo-spatial processing, fluctuating attention and parkinsonism, with higher prevalence of Alzheimer-type lesions in DLB that may account for earlier onset and severity of cognitive deficits. These are also associated with multiple neurotransmitter deficits indicating that cognitive impairment in Lewy body disesses is multifactorial. Recent intra vitam neuroimaging, clinico-pathological studies and animal models suggest that DLB and PDD represent closely related but different, heterogenic subtypes of an α-synuclein-associated disease spectrum (Lewy body diseases) or parts of a continuum with PDD at the mild end of the spectrum, DLB in the middle, and DLB+AD at the more severe end. In view of the controversies about the nosology of both disorders, continuous effort is necessary to differentiate them more clearly and to clarify the underlying pathogenic mechanisms in order to enable effective mechanistic-based treatment, while, currently, no disease-modifying therapies are available.

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White matter hyperintensities on MRI in dementia with Lewy bodies, Parkinson's disease with dementia, and Alzheimer's disease

Cited by 49 publications

References 41 publications

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Oligodendrogliopathy in neurodegenerative diseases with abnormal protein aggregates: The forgotten partner

Neuroimaging and Machine Learning for Dementia Diagnosis: Recent Advancements and Future Prospects

Dementia with Lewy Bodies and Parkinson's Disease-Dementia: Current Perspectives

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