Related Experiment Video

Updated: May 9, 2026

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
10:36

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption

Published on: June 20, 2017

Vascular endothelial growth factor inhibitors and cognitive impairment: evidence and controversies

Terence Ng1, Yin Ting Cheung, Quan Sing Ng

  • 1National University of Singapore , Singapore , Singapore phaac@nus.edu.sg.

Expert Opinion on Drug Safety
|August 13, 2013
PubMed
Abstract

Insights

Targeted cancer therapies, specifically vascular endothelial growth factor inhibitors (VEGFIs), may cause cognitive impairment. More research is needed to understand the link between VEGFIs and brain function in cancer patients.

Area of Science:

  • Neuro-oncology
  • Pharmacology
  • Cognitive Science

Background:

  • Chemotherapy-induced cognitive impairment ('chemobrain') is recognized.
  • Neurocognitive effects of targeted therapies, like anti-angiogenic agents, are understudied.
  • Vascular Endothelial Growth Factor (VEGF) may influence brain cognition, raising concerns about VEGF inhibitors (VEGFIs).

Purpose of the Study:

  • To review mechanisms linking VEGF and cognition.
  • To examine evidence and controversies regarding cognitive issues with VEGFIs.
  • To highlight the potential neurotoxic effects of VEGFIs on cancer patients' cognitive function.

Main Methods:

  • Literature review of existing studies.
  • Analysis of plausible biological mechanisms.
  • Synthesis of current evidence and identification of research gaps.

Main Results:

  • Emerging evidence suggests a potential role for VEGF in cognitive function.
  • VEGFIs are a class of targeted therapies with potential cognitive side effects.
  • The precise impact of VEGFIs on cognitive function remains poorly understood.

Conclusions:

  • VEGFIs may contribute to cognitive changes in cancer patients.
  • Further well-designed studies are necessary to confirm and quantify VEGFI-induced cognitive impairment.
  • Establishing the role of VEGF in human cognition requires more investigation.

More Related Videos

Using Retinal Imaging to Study Dementia09:17

Using Retinal Imaging to Study Dementia

Published on: November 6, 2017

Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions07:30

Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions

Published on: April 23, 2021

Related Concept Videos

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...
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...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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...
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...