22-27, Oct. 2015 

Invitation to IBRC 2015
12th INTERNATIONAL BIOPHILIA REHABILITATION CONFERENCE, Tokyo and Kyoto, Japan; October 22nd - 27th, 2015.



Mieczyslaw Pokorski

Public Higher Medical Professional School in Opole, 68 Katowicka St., 45-060 Opole, Poland

This presentation is designed to give you an overview of the current status of memory function and disorders, and of the molecular basis of memory. I will attempt to demonstrate the possible advantages of clinically-oriented approaches to tackle memory disorders and testing. Memory can be defined as a mental ability to retain information and reconstruct past experience. Memory processing requires complex collaboration of several brain systems; as it involves encoding the information to be remembered, creating a record of the encoded information, and calling it back on a cue. Memory function depends, to a great extent, on psychosomatic health conditions. Organic diseases, which affect bodily organs, disturb memory function. The case in point is here neurodegenerative brain conditions, but any diseased organ, even remotely located from the brain, may affect memory. Psychological disorders, characterized by alterations in thinking, mood, behavior, or associated with distress, also are potent detriments to memory function. The entwined interaction between deteriorating health condition and memory decline is an area of limited understanding. Although ‘health’ is rather a hazy qualification, as it does not have well-defined boundaries, current stratification of memory seems more clear-cut. The basic memory types we currently distinguish are episodic, semantic, procedural, and working memories. This division does not require, as was the case in the past, an arbitrarily set length of short-term or long-term memory. Moreover, each type outlined above has its own fairly specific neuroanatomical localization, and therefore, points to regional brain insufficiency that may be tested.
On the molecular side, glutaminergic neurotransmission is essential for the memory processes. Stimulation of NMDA and AMPA ionotropic receptors by glutamate increases the influx of Ca2+ into the postsynaptic neuron. Calcium/calmodulin-dependent protein kinase II (CaMKII) is an intracellular detector Ca2+ and is now considered the ‘memory switch’ that is responsible for sustained memory of an event after the stimulus that evoked it had ceased to act., CaMKII phosphorylates AMPA channels and helps anchor them to NMDA receptors, perpetuating the events.
Memory disorders are subject to rehabilitation which is now understood as being much broader than just physical rehabilitation due to handicap stemming from diseases such as stroke or iatrogenic causes such as accidents. Rehabilitation, in the modern sense, heavily relies upon motivational aspects expressed by the rehabilitant, i.e., on psychosomatic approaches. There is a paradigm shift in rehabilitation techniques called the motivated rehabilitative exercise. It appears that our understanding of memory shortage and disorders undergoes a similar paradigm shift of late. There is a new stratification of memory and its losses in clinical medicine which goes away from the old-fashioned theories of short and long-term memories. Those old views are arbitrary, confusing, and do not help explain mechanisms underlying memory changes. Nor do they take into account the molecular basis of memory. Science builds up on previous research data and achievements. The only way to the progress, however, is not to be hesitant with advancing new ideas, even if they turn around the old concepts and habits of thinking. Memory rehabilitation is a kind of motivative brain exercise. It also improves the patient’s emotional status raising his self-esteem, which gives the patient a better control over his disease or a better psychological grip on aging. Further exploration of mechanisms involved with memory is essential to obtain a more refined understanding of memory processes.