Scott A. Persohn

The paper evaluates neuro-metabolic and vascular dysregulation in mice post-TBI, finding sex- and injury side-dependent changes that suggest MVD as a potential biomarker.

This study investigates how anti-amyloid immunotherapy affects APOE4 carriers, showing increased glial reactivity, perivascular immune activation, and ARIA-like events.

This study combines clinical cognitive assessments and neuro-metabolic vascular data to predict Alzheimer's disease stage and grade independently of amyloid and tau.

This study uses metabolic covariance analysis on ADNI PET data to identify stage-specific biomarker signatures in Alzheimer's disease progression.

This study identifies neuro-metabolic and vascular dysfunction (MVD) as an early indicator of Alzheimer's disease by analyzing clinical data from ADNI.

This paper characterizes cerebrovascular phenotypes in WSB.APP/PS1 mice, showing age-related CAA, transcriptomic overlap with human AD, myelin deficits, and APOE allele-dependent effects on vascular pathology.

This study characterizes molecular and synaptic changes in a mouse model of late-onset Alzheimer's disease under different dietary conditions, showing age-related brain volume loss and cognitive deficits.

The paper assesses neurovascular uncoupling in APOE variants, finding APOEε4/ε4 shows Type-1 uncoupling and APOEε3/ε4 shows Type-2 uncoupling in aging mice.

This study examines how levetiracetam affects brain metabolic networks and transcriptomic signatures in 5XFAD mice, showing dose- and sex-dependent changes in gene expression and cerebral metabolism.

The paper uses metabolic covariance analysis on PET imaging data from a mouse model of Alzheimer's disease to show age-related metabolic network changes and their alignment with clinical AD stages.

This study examines vascular and metabolic changes in 5xFAD mice over time, finding sex-specific differences in vascular features and glucose metabolism linked to Alzheimer's pathology.

This study creates a mouse model with the MTHFR 677C>T variant and shows it causes cerebrovascular deficits, supporting its use in preclinical research on vascular dementia.

This study shows that a high fat-high sugar diet interacts with the Plcg2M28L genetic variant to accelerate Alzheimer's disease-like phenotypes in mice.