CD2AP loss association with cognitive decline in AD patients

Exploratory Score: 0.850 Price: $0.50 Alzheimer's disease human patients Status: proposed

What This Experiment Tests

Exploratory experiment designed to discover new patterns targeting CD2AP in human patients. Primary outcome: association between vascular CD2AP loss and cognitive decline

Description

Analysis of CD2AP expression in cerebral blood vessels from Alzheimer's disease patients to determine correlation with cognitive decline. This human pathological study examined post-mortem brain tissue from AD subjects to assess whether loss of CD2AP in brain vasculature is associated with cognitive impairment. The study likely used immunohistochemistry or similar techniques to quantify CD2AP protein levels in cerebral blood vessels and correlated these findings with clinical measures of cognitive function obtained prior to death.

TARGET GENE

CD2AP

MODEL SYSTEM

human patients

ESTIMATED COST

TIMELINE

0 months

PATHWAY

cerebrovascular function

SOURCE

extracted_from_pmid_39892386

PRIMARY OUTCOME

association between vascular CD2AP loss and cognitive decline

Scoring Dimensions

📖 Wiki Pages

CD2AP Gene — CD2-Associated Proteingene CD2AP Synaptic Dysfunction Alzheimer's Disease Caumechanism CD2AP Proteinprotein Alzheimer's Disease Genetic Variantsdisease Alzheimer's Disease vs Parkinson's Disease Comparidisease APP Mutations in Alzheimer's Diseasedisease DLB, Parkinson's Disease, and Alzheimer's Disease:disease Early-Onset Alzheimer's Disease (EOAD)disease Investment Landscape: Alzheimer's Diseasedisease Agitation in Alzheimer's Diseasedisease Prodromal Alzheimer's Diseasedisease PSEN1 Mutations in Alzheimer's Diseasedisease PSEN2 Mutations in Alzheimer's Diseasedisease Sporadic vs Familial Alzheimer's Disease: Comprehedisease TREM2 Variants in Alzheimer's Diseasedisease

Protocol

Establish human patients cohorts for Alzheimer's disease and predefine inclusion, exclusion, and quality-control criteria before intervention. 2. Apply the experimental manipulation described for CD2AP, alongside matched control or comparator arms, and document dose, exposure window, and sample timing in a locked protocol log. 3. Measure association between vascular CD2AP loss and cognitive decline together with orthogonal secondary readouts such as molecular, imaging, behavioral, or safety endpoints that are appropriate to the title and study design. 4. Use blinded outcome assessment where feasible, prespecified statistical analysis, and replicate the core readout across biological replicates or an independent validation subset. 5.

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Expected Outcomes

The intervention targeting CD2AP shifts association between vascular CD2AP loss and cognitive decline in the predicted direction relative to the matched control arm.

Secondary disease-relevant readouts in Alzheimer's disease remain directionally concordant with the primary endpoint rather than showing isolated single-assay effects.

The effect persists after adjustment for baseline covariates, batch effects, or repeated-measures structure used in the study design.

Success Criteria

Prespecified primary endpoint (association between vascular CD2AP loss and cognitive decline) improves versus control with p < 0.05 or an equivalent corrected threshold used by the study.
The effect size is biologically meaningful and reproduced across technical/biological replicates or the validation subset.
Safety, data quality, and missingness remain within protocol-defined bounds so the result is interpretable rather than driven by attrition or assay failure.

Related Hypotheses (5)

TREM2-mediated microglial tau clearance enhancement0.618

LRP1-Dependent Tau Uptake Disruption0.600

VCP-Mediated Autophagy Enhancement0.595

Extracellular Vesicle Biogenesis Modulation0.582

HSP90-Tau Disaggregation Complex Enhancement0.575

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