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Aging | Isoform-specific AMPK repression affects cognitive function in aged mice

Peer-Reviewed Publication

Impact Journals LLC

Figure 6

image: Figure 6. Mass spectrometry (MS)-based proteomics analysis reveals distinct alterations of protein expression levels associated with suppression of the neuronal AMPKα isoform in aged mice. view more 

Credit: 2023 Zhou et al.

“The study indicates that the aging process might have distinct impact on the signaling pathways associated with the AMPKα isoforms [...]”

BUFFALO, NY- March 7, 2023 – Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) published a new research paper in Volume 15, Issue 4, entitled, “Isoform-specific effects of neuronal repression of the AMPK catalytic subunit on cognitive function in aged mice.”

AMP-activated protein kinase (AMPK) functions as a molecular sensor that plays a critical role in maintaining cellular energy homeostasis. Dysregulation of the AMPK signaling has been linked to synaptic failure and cognitive impairments. In a recent study, researchers Xueyan Zhou, Wenzhong Yang, Xin Wang, and Tao Ma from Wake Forest University School of Medicine demonstrated abnormally increased AMPK activity in the hippocampus of aged mice. The kinase catalytic subunit of AMPK exists in two isoforms α1 and α2, and their specific roles in aging-related cognitive deficits are unknown. 

“Taking advantage of the unique transgenic mice (AMPKα1/α2 cKO) recently developed by our group, we investigated how isoform-specific suppression of the neuronal AMPKα may contribute to the regulation of cognitive and synaptic function associated with aging.” 

The team found that aging-related impairment of long-term object recognition memory was improved with suppression of AMPKα1 but not AMPKα2 isoform. Moreover, aging-related spatial memory deficits were unaltered with suppression of either AMPKα isoform. Biochemical experiments showed that the phosphorylation levels of the eukaryotic initiation factor 2 α subunit (eIF2α) were specifically decreased in the hippocampus of the AMPKα1 cKO mice. They further performed large-scale unbiased proteomics analysis and revealed identities of proteins whose expression is differentially regulated with AMPKα isoform suppression. These novel findings may provide insights into the roles of AMPK signaling pathway in cognitive aging.

“In summary, the current study reported that suppression of neuronal AMPKα1 isoform can improve aging-related impairments of long-term recognition memory.”


Read the Full Paper: DOI: 

Corresponding Author: Tao Ma

Corresponding Email: 

Keywords: AMPK, aging, protein synthesis, learning and memory, proteomics

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About Aging-US:

Launched in 2009, Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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