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Subchronic effect of a weak combined magnetic field (MF), produced by superimposing a constant component, 42 µT and an alternating MF of 0.08 µT, which was the sum of two frequencies of 4.38 and 4.88 Hz, was studied in olfactory bulbectomized (OBE) and transgenic Tg (APPswe, PSEN1) mice, which were used as animal models of sporadic and heritable Alzheimer’s disease (AD) accordingly. Spatial memory was tested in a Morris water maze on the following day after completion of training trials with the hidden platform removed. The amyloid-β (Aβ) level was determined in extracts of the cortex and hippocampus of mice using a specific DOT analysis while the number and dimensions of amyloid plaques were detected after their staining with thioflavin S in transgenic animals. Exposure to the MFs (4 h/day for 10 days) induced the decrease of Aβ level in brain of OBE mice and reduced the number of Aβ plaques in the cortex and hippocampus of Tg animals. However, memory improvement was revealed in Tg mice only, but not in the OBE animals. Here, we suggest that in order to prevent the Aβ accumulation, MFs could be used at early stage of neuronal degeneration in case of AD and other diseases with amyloid protein deposition in other tissues. [ABSTRACT FROM AUTHOR]

We studied the ability of four non-conjugated α7-subunit fragments of the nicotinic acetylcholine receptor to induce an immune response and to protect memory in olfactory bulbectomized mice which demonstrate abnormalities similar to Alzheimer's disease (AD). Vaccination only with the α7-subunit fragment 173–193 was shown to rescue spatial memory, to restore the level of α7 acetylcholine receptors in the cortex, and to prevent an increase in the amyloid-β (Aβ) level in brain tissue in these animals. Antibodies against the peptide 173–193 were revealed in blood serum and cerebrospinal liquid in the bulbectomized mice. Passive immunization with mouse blood sera containing antibodies to the peptide 173–193 also restored memory in bulbectomized animals. The observed positive effect of both active and passive immunization with the fragment of α7-subunit on memory of bulbectomized mice provides a new insight into an anti-AD drug design. [ABSTRACT FROM AUTHOR]