# Tau networks in AD psychosis

> **NIH NIH K01** · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · 2024 · $106,439

## Abstract

Project Summary/Abstract
The overarching goal of this K01 application is to examine cerebral mechanisms that underlie psychotic
symptoms (PS) in Alzheimer’s disease (AD) using positron emission tomography (PET), diffusion tensor
imaging (DTI), and resting state functional magnetic resonance imaging (rs-fMRI) techniques. I will specifically
address the role of tau pathology and structural and functional network disruptions in the manifestation of PS in
AD. Cerebrospinal fluid (CSF) and post-mortem studies have suggested a role of tau pathology in the
manifestation of PS in AD. However, the cerebral mechanisms that underlie this association remain poorly
understood. A thorough and comprehensive plan for additional training and related career development
activities is proposed based on: 1) Phenomenology of psychosis in the context of AD from both psychiatric and
cognitive perspectives; 2) Tau neurobiology and tau positron emission tomography (PET) imaging; 3) Diffusion
tensor imaging (DTI), tractography, and resting-state functional magnetic resonance imaging (rs-fMRI) network
connectivity. These training goals are intended to provide crucial scientific skills needed to test the following
hypotheses: 1) AD patients with PS will show greater tau accumulation in frontal, cingulate, lateral temporal
and parieto-occipital cortices regions compared to AD without PS; 2) AD with PS will show more abnormal
diffusivity, compared to AD without PS, in white matter tracts that connect frontal, cingulate, lateral temporal,
parietal, and occipital lobes, and functional network connectivity abnormalities in cortical circuits involving the
frontal lobe, specifically the default mode network (DMN) and the salience network (SN); in addition, I expect
that tau aggregation in central nodes of the DMN will correlate with delusions, whereas tau aggregation in the
SN will be associated with hallucinations; 3) Tau aggregation will be greater in the central nodes of these
structural and functional networks in AD patients with PS compared to AD patients without PS; and 4) Tau
aggregation in frontal, temporal and posterior cingulate regions, will correlate with social cognition and
executive function impairments in AD patients with PS. I will use a second generation tau radiotracer ([18F]-
PI2620) that has shown excellent imaging properties and high specificity, in combination with a comprehensive
assessment of both psychiatric (delusions and hallucinations) and cognitive (social cognition and executive
function impairment) manifestations of PS. The proposed combination of training and research plans will lay
the ground to launch my independent career to test neurobiological hypotheses regarding behavioral
manifestations of AD from a neuroimaging perspective.

## Key facts

- **NIH application ID:** 10847474
- **Project number:** 5K01AG078496-03
- **Recipient organization:** FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH
- **Principal Investigator:** Jesus J Gomar
- **Activity code:** K01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $106,439
- **Award type:** 5
- **Project period:** 2022-09-15 → 2027-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10847474

## Citation

> US National Institutes of Health, RePORTER application 10847474, Tau networks in AD psychosis (5K01AG078496-03). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10847474. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*