Effect of White Matter Hyperintensity on Medial Temporal Lobe Atrophy in Alzheimer’s Disease

Jang, Jae‐Won; Kim, SangYun; Na, Hye Yeon; Ahn, Seha; Lee, Sang Jin; Kwak, Ki-Hyeon; Lee, Mina; Hsiung, Ging-Yuek Robin; Choi, Byung-Sun; Youn, Young Chul

doi:10.1159/000345999

Cited by 17 publications

(13 citation statements)

References 27 publications

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“…Previous studies have reported that WMH are associated with an increased risk of dementia (Bocti et al, 2005) and rapid declines in global cognitive function (Ku et al, 2011). Two latest studies proved that periventricular WMH (PWMH) is inversely correlated with hippocampus volume as well as performance of episodic memory in AD patients (Kandiah et al, 2013), and was also inversely correlated with the cognitive deterioration in PD patients (Jang et al, 2013). Further studies, determining the association of RNFL thickness with WMH and other biomarkers of AD, e.g., hippocampus volume, CSF Aβ and/or Tau, are warranted to determine the underlying mechanisms of our clinical observation.…”

Section: Discussionmentioning

confidence: 99%

The attenuation of retinal nerve fiber layer thickness and cognitive deterioration

Shen¹,

Shi²,

Jia³

et al. 2013

Front. Cell. Neurosci.

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Thinner retinal nerve fiber layer (RNFL) has been reported in Alzheimer’s disease (AD) patient. However, whether changes in RNFL thickness can predict the cognitive deterioration remains unknown. We therefore set out a prospective clinical investigation to determine the potential association between the attenuation of RNFL thickness and the deterioration of cognitive function over a period of 25 months. We assessed cognitive function using the Repeatable Battery for the Assessment of Neuropsychological Status and measured RNFL thickness employing optical coherence tomography in 78 participants (mean age 72.31 ± 3.98 years, 52% men). The participants were categorized as stable participants whose cognitive status remained no change (N = 60) and converted participants whose cognitive status deteriorated (N = 18). We found that there was an association between the attenuation of superior quadrant RNFL thickness and the deterioration of cognitive function in the stable participants. In the converted participants, however, there was an inverse association between the reduction of inferior quadrant RNFL thickness and decline of cognitive functions [scores of list recall (R = -0.670, P = 0.002), adjusted (R = -0.493, P = 0.031)]. These data showed that less reduction in the inferior quadrant of RNFL thickness might indicate a higher risk for the patients to develop cognitive deterioration. These findings have established a system to embark a larger scale study to further test whether changes in RNFL thickness can serve as a biomarker of AD, and would lead to mechanistic studies to determine the cellular mechanisms of cognitive deterioration.

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Section: Discussionmentioning

confidence: 99%

The attenuation of retinal nerve fiber layer thickness and cognitive deterioration

Shen¹,

Shi²,

Jia³

et al. 2013

Front. Cell. Neurosci.

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“…Imaging studies have provided evidence for combined involvement of AD and vascular pathology in cognitive decline, and have found an additive effect of WMHs and hippocampal atrophy on MRI, as well as an association between periventricular WMHs and hippocampal atrophy. 107,108 These findings suggest that dementia in older people is often a heterogeneous condition in which different pathologies contribute to the clinical dementia syndrome.…”

Section: Wmhs and The Development Of Dementiamentioning

confidence: 94%

White matter hyperintensities, cognitive impairment and dementia: an update

2015

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White matter hyperintensities (WMHs) in the brain are the consequence of cerebral small vessel disease, and can easily be detected on MRI. Over the past three decades, research has shown that the presence and extent of white matter hyperintense signals on MRI are important for clinical outcome, in terms of cognitive and functional impairment. Large, longitudinal population-based and hospital-based studies have confirmed a dose-dependent relationship between WMHs and clinical outcome, and have demonstrated a causal link between large confluent WMHs and dementia and disability. Adequate differential diagnostic assessment and management is of the utmost importance in any patient, but most notably those with incipient cognitive impairment. Novel imaging techniques such as diffusion tensor imaging might reveal subtle damage before it is visible on standard MRI. Even in Alzheimer disease, which is thought to be primarily caused by amyloid, vascular pathology, such as small vessel disease, may be of greater importance than amyloid itself in terms of influencing the disease course, especially in older individuals. Modification of risk factors for small vessel disease could be an important therapeutic goal, although evidence for effective interventions is still lacking. Here, we provide a timely Review on WMHs, including their relationship with cognitive decline and dementia.

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“…While extensive WMH can drive widespread cortical thinning and ventricular expansion 26–28 , regional WMH load may also be relevant. For example frontal WMH may have a greater impact on frontal lobe thinning 28–31 . On the other hand, locations of the infarctions also have a direct impact on region specific neurodegeneration 32 .…”

Section: Contribution Of Cerebrovascular Pathologies To Neurodegeneramentioning

confidence: 99%

The role of cerebrovascular disease when there is concomitant Alzheimer disease

Vemuri

Knopman

2016

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Cerebrovascular Pathologies (CVP) are the most common co-existent pathologies observed in conjunction with Alzheimer disease. CVP rarely exists in isolation in later life, and CVP most likely plays a supporting role, rather than a sole leading role, in the pathogenesis of dementia. Our goal is to illustrate CVP’s role using neuroimaging biomarkers. First, we discuss the frequency of CVP and present data from population-based Mayo Clinic Study of Aging. Here, we used a novel metric for identifying individuals with cerebrovascular imaging abnormalities (that we designate as “V+”) and present the frequency of V−/V+ in the context of absence and presence of β-amyloid elevation (designated A−/A+). Next, we discuss the contribution of CVP to neurodegeneration and use hippocampal volume loss over time in a subset of participants categorized as A−V−, A−V+, A+V−, A+V+. Lastly, we discuss the contribution of CVP to cognitive impairment and conclude with the considerations for design of future studies.

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Effect of White Matter Hyperintensity on Medial Temporal Lobe Atrophy in Alzheimer’s Disease

Cited by 17 publications

References 27 publications

The attenuation of retinal nerve fiber layer thickness and cognitive deterioration

The attenuation of retinal nerve fiber layer thickness and cognitive deterioration

White matter hyperintensities, cognitive impairment and dementia: an update

The role of cerebrovascular disease when there is concomitant Alzheimer disease

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