Associations between amyloid β and white matter hyperintensities: A systematic review

Roseborough, Austyn D.; Ramirez, Joel; Black, Sandra E.; Edwards, Jodi D.

doi:10.1016/j.jalz.2017.01.026

Cited by 107 publications

(70 citation statements)

References 72 publications

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“…In addition, the previous study measured WM hypointensities using T1-weighted images, which can result in lower volume estimates compared to the 3D FLAIR sequences used here to measure WMH [42]. The lack of association between Ab status and WMH observed in the present study is, however, consistent with reports that Ab and WMH accumulation reflect independent processes whose deleterious effects on cognition are additive [43][44][45].…”

Section: Discussionsupporting

confidence: 83%

Rates of age‐ and amyloid β‐associated cortical atrophy in older adults with superior memory performance

Dang

Yassi

Harrington

et al. 2019

Alz & Dem Diag Ass & Dis Mo

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Introduction Superior cognitive performance in older adults may reflect underlying resistance to age‐associated neurodegeneration. While elevated amyloid β (Aβ) deposition (Aβ+) has been associated with increased cortical atrophy, it remains unknown whether “SuperAgers” may be protected from Aβ‐associated neurodegeneration. Methods Neuropsychologically defined SuperAgers (n = 172) and cognitively normal for age (n = 172) older adults from the Australian Imaging, Biomarkers and Lifestyle study were case matched. Rates of cortical atrophy over 8 years were examined by SuperAger classification and Aβ status. Results Of the case‐matched SuperAgers and cognitively normal for age older adults, 40.7% and 40.1%, respectively, were Aβ+. Rates of age‐ and Aβ‐associated atrophy did not differ between the groups on any measure. Aβ− individuals displayed the slowest rates of atrophy. Discussion Maintenance of superior memory in late life does not reflect resistance to age‐ or Aβ‐associated atrophy. However, those individuals who reached old age without cognitive impairment nor elevated Aβ deposition (i.e. Aβ−) displayed reduced rates of cortical atrophy.

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Section: Discussionsupporting

confidence: 83%

Rates of age‐ and amyloid β‐associated cortical atrophy in older adults with superior memory performance

Dang

Yassi

Harrington

et al. 2019

Alz & Dem Diag Ass & Dis Mo

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“…Considering this, LCN2 may be a valuable biomarker for VaD in the context of differential diagnosis. Such a marker has long been pursued 17,18,34 . Besides new imaging markers that display functional consequences of vascular lesions 29,36 , fluid markers like LCN2 are candidates to contribute to a biomarkerbased definition of VaD as has recently been proposed for AD 7 .…”

Section: Discussionmentioning

confidence: 99%

“…In addition, WMH are frequent in patients with AD 15 and might be caused by neurodegeneration 16 . In summary, new biomarkers are needed to improve diagnosis, to uncover the pathophysiology, and to monitor clinical trials [17][18][19][20] .…”

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confidence: 99%

Cerebrospinal fluid lipocalin 2 as a novel biomarker for the differential diagnosis of vascular dementia

et al. 2020

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The clinical diagnosis of vascular dementia (VaD) is based on imaging criteria, and specific biochemical markers are not available. Here, we investigated the potential of cerebrospinal fluid (CSF) lipocalin 2 (LCN2), a secreted glycoprotein that has been suggested as mediating neuronal damage in vascular brain injuries. The study included four independent cohorts with a total n = 472 samples. LCN2 was significantly elevated in VaD compared to controls, Alzheimer's disease (AD), other neurodegenerative dementias, and cognitively unimpaired patients with cerebrovascular disease. LCN2 discriminated VaD from AD without coexisting VaD with high accuracy. The main findings were consistent over all cohorts. Neuropathology disclosed a high percentage of macrophages linked to subacute infarcts, reactive astrocytes, and damaged blood vessels in multi-infarct dementia when compared to AD. We conclude that CSF LCN2 is a promising candidate biochemical marker in the differential diagnosis of VaD and neurodegenerative dementias.

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“…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). The size of the nuclei of oligodendrocytes is reduced in AD (Gagi et al, 2012).…”

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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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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Associations between amyloid β and white matter hyperintensities: A systematic review

Cited by 107 publications

References 72 publications

Rates of age‐ and amyloid β‐associated cortical atrophy in older adults with superior memory performance

Rates of age‐ and amyloid β‐associated cortical atrophy in older adults with superior memory performance

Cerebrospinal fluid lipocalin 2 as a novel biomarker for the differential diagnosis of vascular dementia

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

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