Ana Catarina Pereira

Plasma p-tau217 and glucose metabolism correlate in neocortical association areas in Alzheimer's disease

Single-Nuclei Transcriptomic Characterization of <i>APOE4</i> -Associated Alzheimer’s Disease

Global multi‐specialty clinician perspectives on the implementation of Alzheimer's disease blood biomarkers

Neocortical tau propagation is a mediator of clinical heterogeneity in Alzheimer’s disease

Molecular signatures of regional vulnerability to tauopathy in excitatory cortical neurons

Apolipoprotein E and Alzheimer's disease pathology in a diverse autopsy study

APOE4 promotes cerebrovascular fibrosis and amyloid deposition via a pericyte-to-myofibroblast transition

Retrotransposon Activation in the Aged and Alzheimer’s Disease Brain Examined by Nanopore Long-read DNA Sequencing

Acceptable performance of blood biomarker tests of amyloid pathology — recommendations from the Global CEO Initiative on Alzheimer’s Disease

Single-cell transcriptomic and neuropathologic analysis reveals dysregulation of the integrated stress response in progressive supranuclear palsy

Common and divergent pathways in early stages of glutamate and tau-mediated toxicities in neurodegeneration

Neuropathologic and transcriptomic analysis reveals abnormal stress response in sporadic progressive supranuclear palsy autopsy brain tissue and human iPSC‐derived midbrain organoids

Modeling the Blood-Brain Barrier Using Human-Induced Pluripotent Stem Cells

Single-cell transcriptomic and neuropathologic analysis reveals dysregulation of the integrated stress response in progressive supranuclear palsy

Investigating mechanisms of sporadic progressive supranuclear palsy in autopsy‐validated human iPSC‐derived midbrain organoids and human brain tissue

Astrocyte-secreted glypican-4 drives APOE4-dependent tau hyperphosphorylation

Neuronal Network Excitability in Alzheimer’s Disease: The Puzzle of Similar versus Divergent Roles of Amyloid β and Tau

Riluzole, a glutamate modulator, slows cerebral glucose metabolism decline in patients with Alzheimer’s disease

Chronic Intermittent Hypoxia Enhances Pathological Tau Seeding, Propagation, and Accumulation and Exacerbates Alzheimer-like Memory and Synaptic Plasticity Deficits and Molecular Signatures

Dysregulation of mitochondrial and proteolysosomal genes in Parkinson’s disease myeloid cells

Differential expression of tau species and the association with cognitive decline and synaptic loss in Alzheimer's disease

Dysregulated coordination of MAPT exon 2 and exon 10 splicing underlies different tau pathologies in PSP and AD

Single-cell atlas of progressive supranuclear palsy reveals a distinct hybrid glial cell population

The epichaperome is a mediator of toxic hippocampal stress and leads to protein connectivity-based dysfunction

Discordant transcriptional signatures of mitochondrial genes in Parkinson’s disease human myeloid cells

Neurotoxic astrocytes secreted glypican-4 drives Alzheimer’s tau pathology

Divergent roles of astrocytic versus neuronal EAAT2 deficiency on cognition and overlap with aging and Alzheimer’s molecular signatures

Sex and age differentially affect GABAergic neurons in the mouse prefrontal cortex and hippocampus following chronic intermittent hypoxia

Correction: Riluzole reduces amyloid beta pathology, improves memory, and restores gene expression changes in a transgenic mouse model of early-onset Alzheimer’s disease

Riluzole reduces amyloid beta pathology, improves memory, and restores gene expression changes in a transgenic mouse model of early-onset Alzheimer’s disease