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The sense of smell is achieved through the activities of the olfactory system. It starts when an airborne odorant enters the nasal cavity and reaches olfactory epithelium (OE). The OE is protected by a thin layer of mucus, which also serves the purpose of dissolving more complex compounds into simpler chemical odorants. The size of the OE and the density of sensory neurons varies among species; in humans, the OE is only about 9-10 cm2.
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    Area of Science:

    • Neuroscience
    • Alzheimer's Disease Research
    • Cognitive Neuroscience

    Background:

    • Alzheimer's disease (AD) involves amyloid beta and neurofibrillary tangles, causing neuronal loss in the entorhinal cortex (EC).
    • The lateral EC (LEC) is vital for non-spatial memory, including object recognition, via object and trace cells.
    • Dysfunction in LEC can lead to memory impairments like forgetfulness and disorientation.

    Purpose of the Study:

    • To investigate the impact of AD pathology on LEC neuronal function and object coding.
    • To assess memory deficits in a transgenic mouse model (EC-App/Tau) mimicking AD-related EC pathology.
    • To correlate neuronal firing patterns with memory performance in the context of AD.

    Main Methods:

    • Utilized a transgenic EC-App/Tau mouse model expressing amyloid precursor protein (APP) and tau in the EC.
    • Performed in vivo single-unit electrophysiology recordings in the LEC of both transgenic and control mice.
    • Assessed performance in LEC-specific memory tasks to evaluate functional deficits.

    Main Results:

    • EC-App/Tau mice exhibited deficits in LEC-specific memory tasks.
    • LEC neurons in transgenic mice showed hyperactivity, low information content, and high sparsity, indicating poor firing fidelity.
    • Object and trace cells in EC-App/Tau mice displayed reduced firing precision, suggesting impaired object encoding.

    Conclusions:

    • AD pathology in the EC leads to aberrant LEC neuronal firing and impaired object coding.
    • These cellular and network-level defects contribute to the non-spatial memory impairments observed in Alzheimer's disease.
    • The EC-App/Tau mouse model provides insights into the mechanisms underlying AD-related memory loss.