Distinct spatial patterns of perivascular spaces enlargement for multiple and Co-existing pathologies of cognitive

Woosik Kim1, Yejin Hwang2, Yelim Yang2

  • 1School of Biomedical Engineering, Korea University, 145, Anam-ro, Seongbuk-gu, Seoul, South Korea; AI Imaging Research Center, NeuroXT, Inc., 48, Achasan-ro 17-gil, Seongdong-gu, Seoul, South Korea.

Abstract

Insights

Vascular pathology increases basal ganglia perivascular spaces (PVS), while amyloid-β and vascular issues affect lobar PVS differently. These findings highlight PVS as a biomarker for cognitive impairment pathways.

Area of Science:

  • Neuroimaging
  • Neuropathology
  • Biomarker Discovery

Background:

  • Cognitive impairment is often associated with amyloid-β and vascular pathologies.
  • Perivascular spaces (PVS) on MRI may reflect glymphatic system dysfunction.
  • Understanding the interplay of these pathologies and PVS is crucial for diagnosis.

Purpose of the Study:

  • To investigate the independent and combined effects of amyloid-β and vascular pathology on regional PVS burden.
  • To determine if PVS patterns differ based on the presence and combination of amyloid-β and vascular pathologies.
  • To assess PVS as a potential imaging biomarker in cognitively impaired individuals.

Main Methods:

  • Retrospective analysis of 307 cognitively impaired participants.
  • Automatic quantification of PVS in basal ganglia and lobar white matter using T2-weighted MRI.
  • Classification of participants based on amyloid-β and vascular pathology status using PET and small vessel disease markers.
  • Statistical analysis using ANCOVA and multivariable linear regression to assess group differences and interactions.

Main Results:

  • Vascular pathology was associated with increased basal ganglia PVS, independent of amyloid-β.
  • Lobar PVS were elevated in participants with single pathologies compared to those with no pathology.
  • Amyloid-β retention correlated with lobar PVS in vascular pathology-negative individuals, while vascular burden correlated with basal ganglia PVS in amyloid-β-negative individuals.
  • Less-than-additive interactions between amyloid-β and vascular pathology were observed for lobar PVS.

Conclusions:

  • Regional PVS patterns are distinct and reflect spatially selective glymphatic alterations.
  • PVS burden is associated with amyloid-β and vascular pathologies in a severity-dependent manner.
  • Perivascular spaces serve as a quantitative imaging biomarker for differentiating mixed pathways contributing to cognitive impairment.

Related Concept Videos

Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Imaging Studies VII: Vascular Imaging01:19

Imaging Studies VII: Vascular Imaging

DefinitionRenal angiography, also known as renal arteriography, is an imaging technique used to obtain a comprehensive view of blood flow and the vascular structure of blood vessels in the kidneys and surrounding areas.PurposeRenal angiography detects blood vessel abnormalities in the kidneys, such as aneurysms, stenosis, thrombosis, vascular tumors, and renal artery stenosis. It evaluates kidney function and guides interventional treatments like angioplasty or stent placement.Pre-Procedure...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...