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Circadian clock gene Rev-erb in memory dysfunction in Alzheimer's disease

Award Number: R01AG069966
ORGANIZATION: NATIONAL INSTITUTE ON AGING
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 02/15/2021
PERIOD OF PERFORMANCE END DATE: 01/31/2027

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Circadian clock gene Rev-erb in memory dysfunction in Alzheimer's disease - ABSTRACT/SUMMARY Abnormal circadian rhythms of locomotor activities, body temperature, and hormonal levels not only are strongly associated many neurodegenerative disorders including Alzheimer’s disease (AD) in both human patients and animal models, but also precede cognitive deficits. However, it is unclear whether and how circadian disruption per se causes cognitive deficits. It is also unclear whether and how the central circadian clock in the suprachiasmatic nucleus (SCN) of the hypothalamus contributes to cognitive functions. Here we found that an AD mouse model (APP NL-G-F) displays disrupted SCN molecular clock, including nuclear receptors Rev-erbα and Rev-erbβ, and these molecular deficits proceed detectable cognitive dysfunctions. Circadian disruptions, either by constant light exposure or by genetic deletion of Rev-erb in the SCN GABAergic neurons, cause cognitive dysfunctions resembling those in APP NL-G-F mice. We hypothesize that disrupted circadian clock in the SCN and alterations in SCN-originated neural circuitry contributes to cognitive dysfunctions in AD. We will determine whether restoration of Rev-erb in the SCN rescues cognitive deficits in APP NL-G-F mice; determine whether rhythmic SCN GABA neuron firing pattern is required to maintain normal cognitive functions; and determine whether the GABA-SCN>PVT circuit regulates cognitive functions. Modern human society is featured with nighttime light, nighttime feeding, social jetlag, and shift work. These circadian disruptions are highly associated with memory deficits and neurodegenerative diseases, especially in aged populations. The proposed study combines unique genetic animal models, light schedule manipulation, precise neuromodulation tools, and cutting-edge molecular methods to address mechanisms of how circadian disruptions cause cognitive deficits. Accomplishing these aims will provide novel insights into the pathophysiology of AD-related dementia, and lay groundwork for chronotherapeutic interventions.


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 = $0 )
2026	2025	BAYLOR COLLEGE OF MEDICINE	1 BAYLOR PLZ	HOUSTON	TX	77030	HARRIS	USA	Aging Research	000	3	12/19/2025	NON-COMPETING CONTINUATION	$0
														Subtotal = $0

Issue Date FY: 2025 ( Subtotal = $559,304 )
2025	2025	BAYLOR COLLEGE OF MEDICINE	1 BAYLOR PLZ	HOUSTON	TX	77030	HARRIS	USA	Aging Research	001	3	8/4/2025	NON-COMPETING CONTINUATION	$45,656
2025	2025	BAYLOR COLLEGE OF MEDICINE	1 BAYLOR PLZ	HOUSTON	TX	77030	HARRIS	USA	Aging Research	000	3	1/9/2025	NON-COMPETING CONTINUATION	$513,648
														Subtotal = $559,304

Issue Date FY: 2024 ( Subtotal = $788,110 )
2024	2024	BAYLOR COLLEGE OF MEDICINE	1 BAYLOR PLZ	HOUSTON	TX	77030	HARRIS	USA	Aging Research	000	2	1/31/2024	EXTENSION WITH OR WITHOUT FUNDS	$513,647
2024	2024	BAYLOR COLLEGE OF MEDICINE	1 BAYLOR PLZ	HOUSTON	TX	77030	HARRIS	USA	Aging Research	002	2	8/7/2024	EXTENSION WITH OR WITHOUT FUNDS	$217,391
2024	2024	BAYLOR COLLEGE OF MEDICINE	1 BAYLOR PLZ	HOUSTON	TX	77030	HARRIS	USA	Aging Research	001	2	7/15/2024	EXTENSION WITH OR WITHOUT FUNDS	$57,072
														Subtotal = $788,110

Grand Total All Awards = $1,347,414

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Circadian clock gene Rev-erb in memory dysfunction in Alzheimer's disease

Award Number: R01AG069966

ORGANIZATION: NATIONAL INSTITUTE ON AGING

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 02/15/2021

PERIOD OF PERFORMANCE END DATE: 01/31/2027

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