Growing evidence suggests an important pathogenetic role of brain-specific gangliosides in the mechanisms underlying Alzheimer’s disease (AD), the most common form of dementia. Nutritional strategies targeting ganglioside sialylation—for example, through agglutinin-mediated modulation—have therefore attracted increasing research interest. In particular, wheat malt extract (WME), a food-derived source of wheat germ agglutinin (WGA) with high affinity for gangliosides, may influence molecular pathways involved in AD pathogenesis. Twelve-month-old female APPswe/PS1E9 transgenic mice, a model of AD, and wild-type (WT) littermates received WME or tap water for three weeks. Behavioral performance was subsequently assessed. Amyloid plaque burden and astrocyte activation were evaluated using Congo red staining and GFAP immunoreactivity, respectively. Gene expression of selected AD markers in the brain was quantified by RT–qPCR. Aged WT mice exhibited robust, region-specific molecular responses to WME, including upregulation of activity-dependent and synaptic plasticity genes (Arc, Egr1, Bdnf, Syp), enhancement of metabolic and insulin-related signaling (Pgc1a, Sirt1, Igf1r, Irs2), increased Cldn5 expression, and reduced pro-inflammatory Il1β expression. APP/PS1 mice exhibited limited response to WME, suggesting more persistent transcriptional signatures of synaptic impairment, metabolic dysregulation, and neuroinflammation than in WT mice. We found no significant effects of WME treatment on amyloid plaque density and behavior in APP/PS1 mice. No effects on astrocyte activation were observed in either group. These findings demonstrate that dietary WME counteracts abnormal behaviors and molecular changes in neuron plasticity, metabolic, and vascular markers under conditions of normal aging but fails to improve the hallmarks of AD pathology. This highlights the potential of WGA-containing nutrients as a preventive nutritional approach targeting pathogenic mechanisms of aging and, potentially, AD pathology.

Introduction. Neuroimplants are devices that interact with the nervous system for recording, stimulating or replacing neural activity. Neuroimplants refer to invasive technologies and are a particular example of brain-computer interfaces that measure brain activity and interpret it to control external devices and computers. This paper will discuss invasive neurointerfaces (IN), their applications, directions of development and limitations of these technologies. Materials and methods. The search was conducted in PubMed, Google Scholar and Scopus databases, as well as in open Internet sources. Results and discussion. This section presents a description of the most common neuroinvasive structures, their applications in neurology, psychiatry, and fundamental research. In neurology neuroinvasive devices are the most widely spread. They significantly increase the effectiveness of treatment of patients with pharmacoresistant forms of migraine and epilepsy, provide rehabilitation of patients after a stroke and allow them to adapt to the performance of everyday tasks. In psychiatry, neuroimplants are used in the form of DBS (deep brain stimulation) devices that reduce the severity of symptoms of mental disorders by acting on functional networks. Conclusion. Neuroimplants provide opportunities for the treatment of pharmacoresistant diseases, such as pharmacoresistant epilepsy, increasing the quality of life of the patients. Current research interest is focused on developing bidirectional signal devices that, by reading brain activity patterns, analyze them and convert them into signals that allow patients to interact with the outside world.