Partner with us Precision medicine for Alzheimer's disease
Right patient.
Right biology.
Better outcomes.
Precision-AD discovers biologically distinct forms of Alzheimer's disease—then turns those insights into targeted therapeutics, companion diagnostics, and smarter clinical trials.
01 — The premise
Alzheimer's is not one disease.
We shouldn't treat it like one.
Today's one-size-fits-all approach obscures the biology that determines who responds, who does not, and which therapeutic strategy belongs in which patient.
02 — Our platform
From human biology
to precision assets.
We integrate human multi-omic and clinical data to find the biology hidden inside an Alzheimer's diagnosis—then design the therapeutic and diagnostic paths together.
Discover
Find reproducible, disease-relevant signals across harmonized genomics, proteomics, imaging, and clinical phenotypes.
- Human-first evidence
- Multi-cohort replication
Stratify
Resolve biologically coherent patient subgroups and the biomarkers that identify them.
- Mechanistic subtypes
- Response hypotheses
Translate
Advance targeted interventions, companion diagnostics, and enrichment strategies around the same biology.
- Therapeutic programs
- Trial-ready biomarkers
The difference
Designed to close
the translation gap.
Human evidence
at the center
Programs begin with disease biology observed in people—not a model looking for relevance.
Therapeutic + diagnostic
by design
We build the intervention and the patient-selection strategy as one translational system.
Value across the
development lifecycle
From target discovery through clinical enrichment, every layer sharpens the probability of success.
03 — Pipeline
A focused path
to patient impact.
Our lead programs extend beyond amyloid and tau to target fundamental biological drivers of Alzheimer's disease, backed by robust human evidence and offering a clear, actionable path to therapeutic intervention.
04 — News & insights
Advancing the science
behind precision medicine.
Selected academic research involving Precision-AD co-founder Timothy Hohman spans vascular, synaptic, white-matter, and neuronal-resilience biology—surfacing diverse mechanisms and therapeutic hypotheses beyond amyloid and tau.
Genetic architecture of the limbic white matter microstructure in aging and Alzheimer's disease
Across seven harmonized cohorts, imaging genetics linked limbic white-matter integrity to oligodendrocyte biology, vascular health, inflammation, and Alzheimer's-relevant outcomes.
Read the publicationRBFOX1 association with age at onset of Alzheimer's disease
Multi-cohort analyses linked variation in RBFOX1—a neuron-specific splicing regulator—to age at disease onset and cognitive phenotypes.
Read the publicationMulti-omic expression of the VEGF family relates to Alzheimer's disease across diverse populations
The largest multi-omic study of the VEGF family across diverse Alzheimer's populations replicated protein-level associations with greater neuropathology.
Read the publicationIncreased neuroplastic activity in the pathogenesis of Alzheimer's disease
CSF GAP-43, a marker of synaptic plasticity, tracked with amyloid and tau biomarker changes, implicating neuroplastic activity in Alzheimer's pathogenesis.
Read the publicationGenetic variation in the Nr1d1 transcription factor binding site shapes metabolism-related protein networks associated with cognitive resilience
Integrated proteomics and genetics identified an NR1D1-centered mitochondrial and metabolic network associated with cognitive resilience in a diverse Alzheimer's mouse panel.
Read the publicationThe effect of Alzheimer's disease genetic factors on limbic white matter microstructure
Genetic signals tied to neurodevelopment, lipid metabolism, and inflammation were associated with microstructural differences across memory-related white-matter tracts.
Read the publicationVascular endothelial growth factor receptor-1 (FLT1) interactions with amyloid-beta in Alzheimer's disease: A putative biomarker of amyloid-induced vascular damage
Higher FLT1 levels in cerebrospinal fluid and post-mortem brain tissue were associated with greater tau pathology, particularly among amyloid-positive individuals.
Read the publicationAssociation of ten VEGF family genes with Alzheimer's disease endophenotypes at single-cell resolution
Single-cell analyses mapped distinct VEGF-family signals across endothelial, microglial, glial, and neuronal populations, including potentially protective neuronal effects.
Read the publication05 — Founding team
Built at the intersection
of data and disease.

Annah Sclafani, PhD
Neuropharmacologist and data scientist using computational approaches to accelerate drug discovery and advance novel therapeutic strategies through translational science and human biology.

Timothy Hohman, PhD
Human geneticist and Alzheimer's researcher at the forefront of multi-omic discovery, revealing disease mechanisms, biomarkers, and precision therapeutic targets.

Start a conversation
Let's build the next
generation of Alzheimer's care.
We're seeking biopharma, diagnostic, research, and investment partners who share our conviction that better patient selection can unlock better outcomes.