title: [Neural mechanisms of memory: synaptic and genomic hypotheses].
abstract: Memorizing of new facts and events means that entering signals produce definite changes within the brain. According to the commonly accepted hypothesis, traces of memory are stored through modifications in the strength of synaptic connections, resulting in formations of new patterns of neural activity. This synaptic hypothesis of memory determines the main direction of experimental studies in the field. It is shown in this review that the synaptic hypothesis can hardly explain the mechanism of long-term (often life-long) memory storage as well as memory resistance to both uncontrolled synaptic activity (epileptic seizures) and various adverse effects on the brain (anesthesia, injury, concussion, etc.). Arguments for an alternative hypothesis are given that long-term memory is mainly formed at the intraneural level through modifications of DNA molecules and associated proteins. This genomic hypothesis allows for a new approach to understanding the etiology ofAlzheimer's disease, whose initial symptom is solely memory impairment.
authors.forename: Iu I
authors.initials: IuI
authors.lastname: Arshavskiĭ
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics / Q000503:physiopathology; D000818:Animals; D001921:Brain / Q000502:physiology*; D004247:DNA / Q000502:physiology*; D005786:Gene Expression Regulation / Q000502:physiology; D023281:Genomics; D006801:Humans; D057567:Memory, Long-Term / Q000502:physiology*; D008959:Models, Neurological; D009434:Neural Pathways / Q000502:physiology; D009473:Neuronal Plasticity / Q000235:genetics*; D009474:Neurons / Q000502:physiology; D013569:Synapses / Q000502:physiology*
chemical_list: D004247:DNA