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Investigating the cellular and circuit mechanisms mediating cognitive deficits following thalamic stroke

Award Number: F31NS145738
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 12/18/2026
PERIOD OF PERFORMANCE END DATE: 12/17/2027

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Investigating the cellular and circuit mechanisms mediating cognitive deficits following thalamic stroke - PROJECT SUMMARY/ABSTRACT Each year, over 12 million individuals worldwide suffer a stroke, and it is estimated that 1 in 4 adults over the age of 25 will experience a stroke in their lifetime. Stroke is a leading cause of death and disability, with approximately 50% of stroke survivors developing post-stroke cognitive impairment (PSCI) within the first year. PSCI can range from mild cognitive dysfunction to dementia. Thalamic strokes, in particular, are a significant contributor to cognitive impairments. The thalamus, a brain region responsible for relaying information to the cortex, plays a crucial role in cognitive processing. Over 90% of patients with a thalamic stroke experience memory and executive dysfunctions. The mediodorsal (MD) thalamus is important for working memory processing and patients with a stroke that includes the MD thalamus typically have impaired recollection, but the exact mechanism remains unknown. The goal of my proposal is to investigate the cognitive deficits that develop after a stroke in the MD thalamus and understand the underlying cellular and circuit mechanisms. My preliminary results indicate that mice with an ischemic stroke in the MD thalamus develop working memory deficits as well as network hyperexcitability in the medial prefrontal cortex (mPFC). The proposed research will help establish a direct link between altered neural activity in the mPFC and working memory deficits caused by MD thalamic stroke (Aim 1), and investigate the mechanistic underpinnings of how the stroke alters the balance between excitation and inhibition in the MD-mPFC pathway, particularly the role of parvalbumin-positive (PV+) interneurons in modulating mPFC activity and memory (Aim 2). This proposal will offer novel insights into the cellular and circuit-level mechanisms that underlie working memory deficits after MD thalamic stroke which could lead to advances in stroke recovery research and targeted therapies aimed at improving cognitive function in stroke patients. All research will be conducted at UCSF and at Gladstone Institutes and will benefit from the wealth of resources and training available at both institutions. They will be enriched by in-house data science and statistics tools and courses, and profit from internal and external collaborations. All experiments will be guided by the mentorship of supervising sponsor Dr. Jeanne Paz, and made available for feedback and presentation at conferences and meetings.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $42,966 )
2026	2026	REGENTS OF THE UNIVERSITY OF CALIFORNIA, SAN FRANCISCO, THE	1855 FOLSOM ST STE 425	SAN FRANCISCO	CA	94103	SAN FRANCISCO	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	6/25/2026	NEW	$42,966
														Subtotal = $42,966

Grand Total All Awards = $42,966

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Investigating the cellular and circuit mechanisms mediating cognitive deficits following thalamic stroke

Award Number: F31NS145738

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 12/18/2026

PERIOD OF PERFORMANCE END DATE: 12/17/2027

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