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Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
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[Changes in the activity of amyloid-degrading metallopeptidases leads to disruption of memory in rats]

N M Dubrovskaia, N N Nalivaeva, S A Plesneva

    Zhurnal Vysshei Nervnoi Deiatelnosti Imeni I P Pavlova
    |December 2, 2009
    PubMed

    Insights

    Prenatal hypoxia and aging impair short-term memory by reducing metallopeptidases neprilysin (NEP) and endothelin-converting enzyme (ECE-1) in the brain cortex. Inhibiting these enzymes further disrupts memory, confirming their critical role in cognitive function.

    Area of Science:

    • Neuroscience
    • Biochemistry
    • Gerontology

    Background:

    • Aging and prenatal hypoxia disrupt short-term memory in rats.
    • These conditions are associated with decreased expression of metallopeptidases neprilysin (NEP) and endothelin-converting enzyme (ECE-1) in the brain cortex.
    • NEP and ECE-1 are key enzymes involved in neuropeptide regulation and beta-amyloid peptide degradation.

    Purpose of the Study:

    • To investigate the role of metallopeptidases NEP and ECE-1 in short-term memory.
    • To determine if inhibiting NEP and ECE-1 affects cognitive function.
    • To explore the link between metallopeptidase activity and memory deficits in aging and prenatal hypoxia models.

    Main Methods:

    • Wistar rats (old and adult) subjected to prenatal hypoxia were assessed for short-term memory.
    • Brain cortex expression and activity of NEP and ECE-1 were measured.
    • Microinjections of phosphoramidon (NEP/ECE-1 inhibitor) and thiorphan (NEP inhibitor) into the sensorimotor cortex were performed.
    • Short-term memory was evaluated using a two-level radial maze test.

    Main Results:

    • Prenatal hypoxia led to decreased NEP and ECE-1 expression and NEP activity in the sensorimotor cortex.
    • Microinjections of phosphoramidon and thiorphan into the sensorimotor cortex significantly disrupted short-term memory.
    • Memory impairment was observed at specific time points after enzyme inhibitor administration.

    Conclusions:

    • Metallopeptidases NEP and ECE-1 are critically involved in maintaining short-term memory function.
    • Reduced expression and activity of these enzymes contribute to cognitive deficits observed in aging and after prenatal hypoxia.
    • Targeting NEP and ECE-1 may offer therapeutic strategies for memory disorders.

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