Related Experiment Video

Updated: Apr 21, 2026

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells

In Vitro Modeling of Down Syndrome Neurogenesis Using Human-Induced Pluripotent Stem Cells

Published on: March 7, 2025

Precision medicine for Alzheimer's disease in Down syndrome

Sonal Sukreet¹, Elise K Kim¹, Melissa Petersen²

¹Departments of Physiology and Neuroscience, Keck School of Medicine of the University of Southern California, San Diego, California, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association

|April 19, 2026

Abstract

Introduction:

Down syndrome (DS) exhibits a genetic form of Alzheimer's disease (AD). We used a blood-based proteomic algorithm to predict cognitive status, treatment responders, and change to vitamin E in DS adults from a completed clinical trial, "Vitamin E in Aged Persons with Down Syndrome," which originally showed no significant cognitive benefit using the primary endpoint cognition (Brief Praxis Test [BPT]).

Methods:

Plasma and extracellular vesicle (EV; astrocytic and neuronal) biomarkers were assayed at baseline and 36 months (n = 138 each). Cognitive response was measured using combined scores from the BPT, vocabulary, and behavior and function DS tests. Support vector machine (SVM) analyses predicted diagnostic and treatment responders and change accuracy.

Results:

SVM classified demented versus non-demented with up to 99% accuracy and predicted treatment response and changes with up to 100% accuracy in plasma and EV.

Discussion:

Our study supports blood-based screening and precision diagnostics for AD therapy in DS.

Keywords:

Alzheimer's disease Down syndrome blood‐based biomarkers endosomal dysfunction precision therapy small extracellular vesicles

More Related Videos

Generalized Psychophysiological Interaction PPI Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease

Generalized Psychophysiological Interaction PPI Analysis of Memory Related Connectivity in Individuals at Genetic Risk for Alzheimer's Disease

Published on: November 14, 2017

Assessment of Spontaneous Alternation, Novel Object Recognition and Limb Clasping in Transgenic Mouse Models of Amyloid-β and Tau Neuropathology

Assessment of Spontaneous Alternation, Novel Object Recognition and Limb Clasping in Transgenic Mouse Models of Amyloid-β and Tau Neuropathology

Published on: May 28, 2017

Related Concept Videos

Alzheimer Disease l: Introduction

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's Disease: Treatment

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's Disease: Overview

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...

Alzheimer Disease ll: Pathophysiology

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...

Articles linked to this work by shared authors, journal, and citation graph.

Delayed Recognition and Stroke-Predominant Presentation in Down Syndrome-Associated Moyamoya Syndrome.

Stroke·2026

Blood biomarkers predict conversion from cognitively stable to mild cognitive impairment or Alzheimer's disease in Down syndrome at 16-month follow-up in ABC-DS.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026

Depression and hippocampal subfield volume in older adults.

Translational psychiatry·2026

Relationships between longitudinal retinal amyloid imaging and amyloid PET in the A4 Trial.

Alzheimer's & dementia (Amsterdam, Netherlands)·2026

Exploring automated plasma phospho-tau217 assays for the diagnosis of Down syndrome-related Alzheimer's disease.

Communications medicine·2026

Pre-analytical guidelines for blood and CSF Biomarkers 2025: Recommendations from the NACC ADRC Biofluid Biomarker Best Practices Workgroup.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2026

See all related articles