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    Persistent integrated stress response (ISR) activation impairs memory. A viral protein, DP71L, inhibits ISR, protecting against cognitive decline and enhancing memory in various conditions.

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    Area of Science:

    • Neuroscience
    • Molecular Biology
    • Genetics

    Background:

    • The integrated stress response (ISR) is crucial for cellular homeostasis and cognitive function.
    • A specific genetic variant (PPP1R15B R658C) is linked to intellectual disability and chronic ISR activation.
    • Understanding ISR's role in cognitive function is vital for developing therapeutic strategies.

    Purpose of the Study:

    • To investigate the impact of persistent ISR activation on cognitive performance using a novel mouse model.
    • To explore the therapeutic potential of viral ISR inhibitors for cognitive disorders.

    Main Methods:

    • Generation of a mouse model mimicking the human PPP1R15B R658C variant.
    • Molecular and structural analyses of the viral protein DP71L.
    • Assessment of cognitive performance, protein synthesis, and synaptic plasticity in mice.

    Main Results:

    • The PPP1R15B R658C variant causes chronic ISR activation, impairing protein synthesis and long-term memory.
    • Cognitive and synaptic deficits in the mouse model are directly caused by ISR activation.
    • The viral protein DP71L acts as a potent pan-ISR inhibitor.
    • DP71L ameliorates cognitive decline in models of Down syndrome, Alzheimer's disease, and aging, and enhances memory in healthy mice.

    Conclusions:

    • Chronic ISR activation due to genetic variants like PPP1R15B R658C leads to cognitive deficits.
    • The viral protein DP71L offers a promising therapeutic avenue for treating cognitive decline and enhancing memory.
    • Evolutionary insights can guide the development of novel treatments for neurological disorders.