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Related Concept Videos

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 Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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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...
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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...
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...
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Cognitive Development During Adulthood

Cognitive development continues throughout adulthood, undergoing significant shifts across early, middle, and late stages. Individual transition occurs from adolescent idealism to pragmatic and adaptable thinking in early adulthood. During this period, individuals learn to integrate personal beliefs with the recognition that other perspectives are equally valid. Exposure to the complexities of modern society, diverse experiences, and higher education contribute to this adaptive thought process,...

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Updated: Jun 13, 2026

Dual-Task Stroop Paradigm for Detecting Cognitive Deficits in High-Functioning Stroke Patients
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Published on: December 16, 2022

Assessing Cognitive Deterioration After COVID-19 Infection (The ACDC Study): An Exploratory Multimodal Neuroimaging

Jonathan McLaughlin1, Gordon Waiter2

  • 1Department of Psychological Medicine, NHS Grampian, Ashgrove House, Aberdeen Royal Infirmary, Aberdeen AB25 2ZN, UK.

Journal of Clinical Medicine
|June 12, 2026
PubMed
Summary
This summary is machine-generated.

Cognitive difficulties after COVID-19 show subtle neural changes, not fully explaining "brain fog." Findings suggest a mix of mild neurobiological effects and functional cognitive processes contribute to persistent symptoms.

Keywords:
cognitive impairmentfunctional cognitive disorderfunctional neurological disordermagnetic resonance spectroscopyneuroimaging biomarkerspost-COVID-19 condition

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

Published on: April 23, 2021

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Last Updated: Jun 13, 2026

Dual-Task Stroop Paradigm for Detecting Cognitive Deficits in High-Functioning Stroke Patients
07:42

Dual-Task Stroop Paradigm for Detecting Cognitive Deficits in High-Functioning Stroke Patients

Published on: December 16, 2022

Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions
07:30

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

Published on: April 23, 2021

Area of Science:

  • Neuroscience
  • Neurology
  • Radiology

Background:

  • Cognitive difficulties, including attentional and executive dysfunction, are common after SARS-CoV-2 infection.
  • The neurobiological basis of cognitive symptoms in post-COVID-19 condition (PCC) remains unclear.
  • The relationship between subjective cognitive complaints and objective neurobiological changes in PCC is uncertain.

Purpose of the Study:

  • To investigate the neurobiological underpinnings of persistent cognitive difficulties following hospitalization with COVID-19.
  • To compare neuroimaging and neurochemical data in individuals with PCC to healthy controls.
  • To explore the association between objective neural changes and subjective cognitive symptom severity.

Main Methods:

  • Adults with PCC underwent neuropsychological testing and 3 Tesla MRI, including volumetric imaging, diffusion tractography, and magnetic resonance spectroscopy (MRS) of frontal white matter.
  • Data were compared with age- and sex-matched pre-COVID-19 controls and normative MRS datasets.
  • Analyses adjusted for intracranial volume, sex, and time since infection, with false-discovery-rate correction.

Main Results:

  • Participants showed selective impairments in attention, working memory, and verbal fluency.
  • No widespread volumetric or white-matter differences were found; however, reduced posterior hypothalamic volume and altered occipito-parietal connectivity were observed.
  • MRS revealed reduced N-acetylaspartate and elevated choline, myo-inositol, and glutamate-glutamine ratios; no significant associations were found between imaging measures and cognitive outcomes.

Conclusions:

  • Post-COVID-19 condition exhibits circumscribed cognitive changes and subtle neural differences, but these do not strongly correlate with subjective symptom severity.
  • The mismatch between objective findings and subjective experience suggests that post-COVID-19
  • brain fog