Update on Vascular Cognitive Impairment Associated with Subcortical Small-Vessel Disease

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Wallin, Anders,1950Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology (author)

Update on Vascular Cognitive Impairment Associated with Subcortical Small-Vessel Disease

Article/chapterEnglish2018

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2018

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LIBRIS-ID:oai:gup.ub.gu.se/266597
https://gup.ub.gu.se/publication/266597URI
https://doi.org/10.3233/JAD-170803DOI

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Language:English

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Subject category:for swepub-publicationtype

Notes

Subcortical small-vessel disease (SSVD) is a disorder well characterized from the clinical, imaging, and neuropathological viewpoints. SSVD is considered the most prevalent ischemic brain disorder, increasing in frequency with age. Vascular risk factors include hypertension, diabetes, hyperlipidemia, elevated homocysteine, and obstructive sleep apnea. Ischemic white matter lesions are the hallmark of SSVD; other pathological lesions include arteriolosclerosis, dilatation of perivascular spaces, venous collagenosis, cerebral amyloid angiopathy, microbleeds, microinfarcts, lacunes, and large infarcts. The pathogenesis of SSVD is incompletely understood but includes endothelial changes and blood-brain barrier alterations involving metalloproteinases, vascular endothelial growth factors, angiotensin II, mindin/spondin, and the mammalian target of rapamycin pathway. Metabolic and genetic conditions may also play a role but hitherto there are few conclusive studies. Clinical diagnosis of SSVD includes early executive dysfunction manifested by impaired capacity to use complex information, to formulate strategies, and to exercise self-control. In comparison with Alzheimer's disease (AD), patients with SSVD show less pronounced episodic memory deficits. Brain imaging has advanced substantially the diagnostic tools for SSVD. With the exception of cortical microinfarcts, all other lesions are well visualized with MRI. Diagnostic biomarkers that separate AD from SSVD include reduction of cerebrospinal fluid amyloid-β (Aβ)42 and of the ratio Aβ42/Aβ40 often with increased total tau levels. However, better markers of small-vessel function of intracerebral blood vessels are needed. The treatment of SSVD remains unsatisfactory other than control of vascular risk factors. There is an urgent need of finding targets to slow down and potentially halt the progression of this prevalent, but often unrecognized, disorder.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Psykiatri hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Psychiatry hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Cell- och molekylärbiologi hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Cell and Molecular Biology hsv//eng
Cerebral small vessel disease
Cerebrospinal fluid
Classification
Cognitive impairment
Diagnostic imaging
Genetics
Metabolism
Pathology
Pathophysiology
Symptoms

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Román, G. C. (author)
Esiri, M. (author)
Kettunen, PetronellaGothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology(Swepub:gu)xketpe (author)
Svensson, Johan,1964Gothenburg University,Göteborgs universitet,Institutionen för medicin,Institute of Medicine(Swepub:gu)xsjohc (author)
Paraskevas, G. P. (author)
Kapaki, E. (author)
Göteborgs universitetInstitutionen för neurovetenskap och fysiologi (creator_code:org_t)

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