الفهرس 
Types and classifications of memory systemsOnly 14 pages are availabe for public view
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Abstract
Memory is an array of interacting Systems , each capable of encoding or registering information, storing it, and making it available by retrieval. There are three main stages in the formation of memory: encoding , storage and retrieval. Memory can be classified into: physiological (sensory, primary and secondary), psychological (declerative non declarative , associative non associative , refrence working) and clinical classification (immediate, recent and remote).
Sensory memory is called : immediate memory and divided into: iconic, echoic and memory for non-symbolic stimuli. Primary (short-term) memory is the memory of information for a few seconds and based on reverberation of neuronal circuits. Secondary ( long-term) memory can be recalled at hours to years . The process of storing information is called consolidation and it begain as soon as second.
Declarative (explicit) memory requires conscious awareness of past experience. It is subdivided into: episodic (refers to the memory for events happened at a particular time in a person’s life) and semantic memory (refers to knowledge of organized information). Non Declarative (implicit) memory in contrast to explicit memory refers to recollection of skills and physical operations, procedures that can be remembered automatically and without conscious awareness.
Associative memory includes much of the learning we do. It is generally subdivided into classical and instrumental conditioning or learning while non - associative memory involves the simplest and most primitive forms of learning habituation and sensitization.
Working memory is described as a system that temporarily stores visual and / or auditory information. It is broken down into: the visuospatial sketchpad, the phonological loop and the central executive system.
Many structures are involved in memory including: Hippocampus, temporal lobe, amygdale and ancus, diencephalon , basal forebrain, frontal Lobe , basal ganglia and entorhinal Cortex.
Hippocampus plays an important role in memory. Patients such as HM and RB with damage to the medial temporal lobe (hippocampal region) show anterograde amnesia, which is characterized by inability to form new declarative memories but sparing of older memories, intelligence, attention, and personality. Anterograde amnesia is often accompanied by some degree of retrograde amnesia, loss of memories formed just before the trauma.
Etiologies that can result in anterograde amnesia include stroke, anoxia or hypoxia, herpes encephalitis, normal aging, and Alzheimer’s disease, all of which can damage the hippocampus and nearby structures.
The entorhinal cortex is a periallocortical structure within the hippocampal region, meaning that its form is intermediate between six-layered neocortex and two-layered allocortex. It receives highly processed, multimodal sensory input and projects to the hippocampus; in turn, hippocampal outputs project to entorhinal cortex and from there back to the cortical areas where they arose.
On some tasks, memory impairment simply grows as a function of how much hippocampal region tissue is lesioned. The cortico-hippocampal model suggests that this entorhinal compression may survive selective hippocampal damage, which disables a normally competing hippocampal differentiation function. The result is that selective hippocampal lesion results in a tendency to over compress information, and this is consistent with existing data.
The short - term memory storage requires a neuronal mechanism that can hold specific information signals for a few seconds to a minute or more. It could be mediated by a variety of short-term neural plastic events such as post tetanic potentiation and reverberating circuit.
Theory of short - term memory holds that a tetanic stimulus of a synapse for a few seconds causes a short period of synaptic fatigue for the next few seconds, but then increased excitability of the synapse for another few seconds to a few hours. If during this time of increased excitability the synapse is stimulated again, the neurone responds much vigorously than normal , a phenomenon called post tetanic potentiation (caused by excessive accumulation of ca++in presynaptic terminals ) while the reverberating circuit stops as a result of fatigue of synaptic transmission or by inhibitory impulses from other parts of the central nervous system.
Long - term memory does not depend on continued activity of the nervous system because the brain can totally be inactivated by cooling, general anesthesia, hypoxia and ischemia. Consolidation of memory is aided by
rehearsal of the same information and this potentiates the degree of transfer of primary memory to secondary memory and therefore accelerates and
potentiates the process of consolidation. During this process, similar information is recalled from the secondary storage lines and is used to help process the new information.
Left frontal cortex has been associated with encoding of verbal materials. Memory formation relies on multiple streams of information, most often distinguished as verbal and nonverbal codes. Pictures are associated with both nonverbal (image-based) and verbal codes, whereas words are associated with only a verbal code.
The frontal cortex and the basal ganglia interact via a relatively well understood and elaborate system of interconnections. In the context of motor function, these interconnections can be understood as disinhibiting, or “releasing the brakes,” on frontal motor action plans.
An active gating mechanism dynamically regulates the influence of incoming stimuli on the working memory system. When the gate is open, stimulus information is allowed to flow strongly into the working memory system while when the gate is closed, stimulus information does not strongly influence working memory.
The basal ganglia and the cerebellum have long been known to be involved in motor control because of the marked motor deficits associated with their damage. Traditionally, the cerebellum was supposed to be involved in real-time fine tuning of movement, whereas the basal ganglia were thought to be involved in the selection and inhibition of action commands.
Both basal ganglia and the cerebellum have recurrent connections with the cerebral cortex. Anatomical studies using transneuronally transported viruses have clearly shown that the projections from the basal ganglia and the cerebellum through the thalamus to the cortex constitute multiple ‘parallel’ channels.
There are various neurotransmitters affecting memory. These neurotransmitters are picked up by receptors in the receiving neuron’s dendrites. The receiving neuron integrates all the information it receives from all its afferents and may produce output in turn, releasing neurotransmitters from its own axon. Some neurotransmitters have an excitatory effect on the receiving neuron while others neurotransmitters have an inhibitory effect.
Acetylcholine has a number of neuromodulatory effects. Application of acetylcholine itself can lead to a general increase in activity in pyramidal neurons. In addition, ACh appears to facilitate synaptic plasticity and hence to facilitate learning. Also disruption of the cholinergic system can have a devastating effect on memory.
Cholinergic depletion may underlie some of the cognitive impairments associated with AD. So, there is some similarity between the kinds of memory impairments seen in individuals who are given cholinergic antagonists (such as scopolamine) and individuals in the early stages of AD.
Dopaminergic neuromodulation projecting from prefrontal cortex and basal ganglia seems to exert a critical influence on working memory. Basal ganglia and dopamine are believed to be involved in helping protect memories against these sources of noise, for instance through gating. Dopamine effectively locks this gate by influencing the stability of up and down states in the striatum.
The degradation of dopamine-releasing neurons, both in humans afflicted with Parkinson’s disease and in animal models utilizing pharmacological lesions, leads to deficit in WM, while low doses of systemically delivered dopamine agonists can enhance WM.
Serotonin has an important role in the cognitive processes of learning
and memory. Depletion of brain serotonin levels using the serotonin synthesis inhibitor, p-chlorophenylalanine (PCPA), has either no effect on water maze acquisition, or produces mild impairment in performance.
While the a2 adrenoceptor system has generally been implicated in attentional processing, there have been various reports of therapeutic effects of both a2 agonists and antagonists in patients generally believed to suffer from memory dysfunction.
The medial septum projects GABA as well as ACh to the hippocampus.When the medial septum is lesioned or disrupted, this GABAergic projection to hippocampus is also affected. GABA is the major inhibitory transmitter in the brain, meaning that it tends to reduce activity in the postsynaptic neuron.
Like serotonergic drugs, the benzodiazepines (BZs) have effects both on mood and memory. The actions of BZs are closely linked to those of the inhibitory neurotransmitter GABA since BZ binding sites are located on the GABAA receptor complex. This results in the existence of a synergistic relationship between GABA and BZs.
Some neuropeptides as opiate, vasopressin, oxytocin and neurope¬ptides which are found in CSF and in the limbic regions have been shown in some experiments to be capable of increasing performance in learning and memory tests. Some of these neuropeptides act as modulatory neurotransmitters. They facilitate or inhibit the flow of information, along the neurons of those regions which are important in memory processes.
The muscarinic acetylcholine receptor (mAChR) family has five members that participate in critical cholinergic functions including learning, memory and attention. Five subtypes of mAChRs, M1, M2, M3, M4 and M5, have been revealed by molecular cloning.
The nicotinic cholinergic system has been widely implicated in mediating memory processes in human and nonhuman animals. Stimulation or blockade of nicotinic acetylcholine receptors (nAChRs) has been shown to affect animals performance in a variety of tasks thought to measure memory.
NMDA receptors in the hippocampus proved to have a role in memory process. There is evidence to suggest that long term potentiation of synaptic transmission in the hippocampus is maintained. Since the induction of LTP in hippocampal areas and dentate gyrus is triggered post synaptically by the entry of ca** through ions channels linked to NMDA receptors.
ACTH and glucocorticoides also affect learning and memory . Low doses of ACTH given immediately after a new learning task enhance retention, while 10-fold higher dose has the opposite effect. ACTH also delays extinction of the avoidance response. The effect of ACTH on learning and memory are mediated through the hippocampus and amygdala.
Assessment of memory function includes: Neuropsychological assessment
(Wechsler memory scale, The wechsler Adult intelligence Scale , Memory for designs tests, Tests for verbal and non verbal memory, New learning capacity, Tests of remote memory, Memory self –reports, Tests of meta- memory and The Mini - Mental state Examination) , Neurophysiological assessment (Electroencephalography, Mild cognitive impairment and Evoked potential ), Neuro imaging (Regional cerebral Blood Flow , CT SCAN , MRI , PET SCAN and SPECT) and CSF markers.
The wechsler Adult intelligence Scale (WAIS) may be helpful in distinguishing between the effect of dementia and those of normal aging while Memory for designs tests are more sensitive that immediate recall of digits as behavioral measures of brain damage.
The California verbal learning test provides an apportunity to compare long- term memory under conditions of high and low interference. Visuospatial material has generally been employed to test non verbal memory using both recall and recognition procedures.
EEG in patients with dementia show an accentuation of all these changes and slowing dominantly in the occipital rhythm with non reactivity of background pattern. It was found that healthy elderly subjects who had MCI also had markedly reduced power in all brain regions. MCI patients who later developed obvious dementia had abnormalities of EEG coherence and power when compared with MCI patients who remained stable.
An evoked potential (EP) is the sequence of EEG changes following a sensory stimulus. If the stimulus is repeated, the specific EEG pattern related to it can be discerned by ‘averaging’ the responses and removing the effects of spontaneous background activity.
Sensitive biological markers must be a prerequisite for the diagnosis of early forms of dementia disorders. Several candidates are presently evaluated, including genetic, neuroimaging (structural and functional imaging) and cerebrospinal fluid (CSF) markers (Ab, tau).
Among the CSF markers, increased tau values have been measured in CSF of AD patients, but increased tau levels are also found in other forms of dementia and neurological disorders. Decreased levels of CSF Ab1±42 are mainly found in patients with AD. Combined analysis of tau and Ab1±42 in CSF might be a useful tool in the future to identify early cases of Alzheimer’s disease.
AD shows a decreased flow in parietal, parieto-occipital and parieto¬temporal regions with evidence of reduced flow response to mental activation. Also, CT scan, MRI, PET scan and SPECT have very important role in diagnosis of memory.
Memory disorders may be: qualitative (distortion of recall and distortion of recognition) or quantitative (hyperamnesia and amnesia). Amnesia is classified into: Psychogenic (anxiety, catathymic and hystrical) and organic (acute, subacute and chronic).
Chronic amnesia (Progressive amnestic syndromes): Alzheimer’s Disease , Fronto- temporal dementia, Semantic dementia, Vascular dementia, Lewy Body dementia and Prion disease.
Alzheimer’s Disease is the most common cause of dementia . Symptoms include memory problems, a progressive deterioration in the ability to perform basic activities of daily living and behaviour changes mainly apathy and social withdrawal, but also behavioural disturbances. Alzheimer’s disease causes abnormal function and eventual death of selected nerve cells in the brain. The average survival period for patients following diagnosis is eight to 10 years.
In the past, fronto temporal dementia was used synonymously with Pick’s disease, according to current nosology, FTD encompasses multiple dementing illnesses, including corticobasal ganglionic degeneration and progressive supranuclear palsy.
Semantic dementia is a distinctive clinical syndrome that arises from circumscribed degeneration of the temporal lobes. It is one of a number of distinct syndromes, which include fronto temporal dementia and primary progressive non-fluent aphasia, encompassed within the pathological rubric of fronto temporal lobar degeneration. The disorder is characterized by a progressive loss of semantic (conceptual) knowledge about the world.
On the other hand, vascular dementia is the group of dementias result from strokes destroying areas of the brain that subserve memory and intelligence. These events can be acute, or can take place more gradually and cumulatively. Dementia may follow several small strokes (multi-infarct dementia), or a single infarct or inadequate blood flow (ischaemia) to a critical brain area. In subcortical vascular dementia, ischaemic changes take place in the deep white matter of the cerebral hemispheres.
As in the case of FTD, recent classification schemes have tried to “lump” rather than “split” disorders that are unified by having both dementia and Parkinsonism (bradykinesia, resting tremor, gait instability, rigidity) as their key clinical characteristics, and Lewy bodies in both the subcortex and neocortex as their histological characteristics. The term Lewy body dementia is now commonly used to encompass both Parkinson’s disease with dementia and dementia with Lewy bodies.
Prion diseases are neurodegenerative disorders caused by the transmissible particles that contain a pathogenic isoform of the prion protein. The most common prion apathy is Creutzfeldt-Jakob disease (CJD), which is further subdivided based on modes of transmission: sporadic CJD, iatrogenic CJD, and variant CJD.