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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...
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...
Dementia l: Introduction01:22

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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 (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...

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Related Experiment Video

Updated: Jul 4, 2026

Basics of Multivariate Analysis in Neuroimaging Data
06:35

Basics of Multivariate Analysis in Neuroimaging Data

Published on: July 24, 2010

Cognitive and Neuroimaging Biomarker Intra-Individual Variability in Alzheimer's Disease.

Min Huey Teo, Malcolm Ren Qing Taong, Cheuk Ni Kan

    Medrxiv : the Preprint Server for Health Sciences
    |July 3, 2026
    PubMed
    Summary

    Greater cognitive intra-individual variability (IIV) is linked to increased Alzheimer's disease (AD) biomarker heterogeneity. This association is more pronounced in individuals with mild cognitive impairment (MCI) and existing AD pathology.

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    Area of Science:

    • Neuroscience
    • Biomarkers
    • Cognitive Aging

    Background:

    • Cognitive intra-individual variability (IIV) signifies inconsistent performance across cognitive domains.
    • Increased cognitive IIV is associated with a higher risk of Alzheimer's disease (AD).
    • The relationship between cognitive IIV and the spatial distribution of AD pathology remains under-explored.

    Purpose of the Study:

    • To investigate the association between cognitive IIV and the heterogeneity of AD neuroimaging biomarkers.
    • To explore how this association differs between cognitively normal (CN) and mild cognitive impairment (MCI) individuals.
    • To examine the influence of biomarker positivity on the cognitive IIV-biomarker IIV relationship.

    Main Methods:

    • Utilized data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort.
    • Calculated cognitive IIV from neuropsychological test z-scores.
    • Derived biomarker IIV metrics for amyloid-β, tau, cortical thickness, and the ATN (amyloid-tau-neurodegeneration) score.
    • Employed linear regression models to assess associations, adjusting for covariates.

    Main Results:

    • Higher cognitive IIV correlated with greater IIV in amyloid-β, tau, cortical thickness, and ATN biomarkers.
    • The association between cognitive IIV and biomarker IIV was stronger in MCI than CN participants.
    • Cognitive IIV's link to tau IIV persisted even in tau-negative individuals, while the amyloid-β IIV association was attenuated in amyloid-negative individuals.

    Conclusions:

    • Elevated cognitive IIV is linked to increased heterogeneity in the cortical distribution of AD pathology.
    • This association is particularly evident in prodromal AD (MCI) and when AD pathology is present.
    • AD biomarker IIV offers potential utility in research and clinical settings for assessing pathological scattering beyond absolute biomarker levels.