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Memory (biological)

Memory
Wikipedia resources

Memory
Mnemonic
Declarative memory
HM (amnesia patient)
Anterograde amnesia
Retrograde amnesia
Hippocampus
Place cells
Procedural memory
Short-term memory
Long-term memory
Alzheimer's disease
Memory and aging
Long-term potentiation
Synaptic plasticity
CREB protein

Welcome to the Wikiversity learning project for biological memory. The project allows participants to explore how animal brains store and use memories with special emphasis on health related issues involving human memory.

Introduction

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This project explores questions such as

  1. are there foods, dietary supplements, drugs or exercises that help human memory?
  2. are there drugs and other medical treatments that damage memory?
  3. is there evidence of genetic differences in human memory abilities?
  4. is memory loss a normal aspect of aging?
  5. how can laboratory animals be used to help produce an understanding of human memory?
  6. can knowledge of human memory physiology be used to produce new types of memory systems for artificial intelligence research?
 
Figure 1. We feel that we know our own memories, but introspection does not reveal the brain regions that make memories possible or how they work. Red: location of the Hippocampi of the human brain; key structures required for some types of memory storage.

Types of memory

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You can be consciously aware of some of the memories stored by your brain, but introspection is not a very useful tool for learning about the details of how brains store and use memories. It is important to realize that many of your memories are not available to you by way of conscious recall. Biologists make a distinction between memories that you can be aware of and memories that influence your behavior by acting outside of your conscious awareness[1].

The discovery and study of the many different human brain memory systems is an active area of neurobiology research. Many different terms have been used to refer to different types of human memory and it is not clear that neuroscience yet has the equivalent of a table of the elements of memory. General terms used for discussion of consciously recalled memories are "explicit memory" and "declarative memory". General terms for unconscious memories are "implicit memory", "nondeclarative memory" and "procedural memory". Declarative memory is the basis of our "conscious knowledge about facts and events"[2]. The next section, below, explores evidence from studies of human patients indicating that declarative memory storage is made possible by several specific parts of the brain. Diseases that damage those brain areas can cause patients to lose their normal ability to store new declarative memories.

Examples. If you can remember a phone number or a zip code then those are good examples of explicit memories. Your explicit memories include memories of your past experiences. In general, anything from your past that you can consciously remember, think about and talk about is an explicit memory. What is meant by memories that we cannot consciously recall and describe? Many human behaviors involve skills that we have learned. Our brains allow us to learn many behavioral skills and remember how to perform many tasks but we are not consciously aware of the memories that allow us to do many common tasks such as walk, write or ride a bike.

 
Figure 2. The part of the brain shaded green in this diagram indicates the temporal lobe of the human cerebrum. Parts of the brain in and near the temporal lobe are important for storage of new declarative memories. In Figure 1 (above), note that the hippocampi are located under the cerebral cortex that is at the surface of the temporal lobes.

Anatomical brain regions involved in memory storage

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Parts of the temporal lobe and the diencephalon are particularly important for the storage of new declarative memories. The importance of these specific brain regions for memory storage was first revealed by studies of human patients who had suffered damage to these parts of the brain. Damage to specific parts of the brain can be caused by strokes or some types of brain infections. Also, the temporal lobes are the center of abnormal neuronal activity in some patients with epilepsy and in some cases surgical removal of the temporal lobes has been performed.[2]

The most famous case of a patient with brain damage resulting in disruption of formation of new declarative memories is "H.M." who suffered from severe temporal lobe epilepsy.[3] In an attempt to treat the epilepsy, Scoville and Milner removed brain tissue from both sides of the patient's brain. The removed brain tissue was at the inner side of the temporal lobe. The operation resulted in a specific memory defect. H.M. could still form new procedural memories and short-term declarative memories, but long-lasting declarative memories could no longer be demonstrated.

The distinction between short-term memory and Long-term memory was evident in H.M.'s behavior after his surgery. H.M. retained an ability to recall facts and experiences from the past few minutes, but was no longer able to recall new experiences from one day to the next.

Read and discuss

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Clinical Cases That Reveal the Anatomical Substrate for Declarative Memories - Three short case descriptions from the online textbook Neuroscience (Second Edition) by Dale Purves et al (2001).

Questions and comments

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Drugs and memory

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Alzheimer disease is a neurodegenerative disease and the most common cause of dementia. Reduced declarative memory formation is often an early indicator of Alzheimer disease. A recent study concluded that atrophy of the hippocampus measured by magnetic resonance imaging can predict dementia [4]

Cholinergic hypothesis

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The cholinergic hypothesis of Alzheimer disease is the idea that cholinergic neurotransmission has a special role brain regions that are important in attention and memory. For example, it may be that frontal cortex activity needs to be coupled to temporal lobe activity in order to allow efficient function of the hippocampus for memory formation. Cholinesterase inhibitors are used clinically as a part of Alzheimer disease treatment.

There has been interest in the idea that the earliest indications of decline in memory function might be an indication of neurodegeneration that involves reduced cholinergic neurotransmission[5].

  • tacrine (Cognex®), approved in 1993
  • donepezil (Aricept®), approved in 1996
  • rivastigmine (Exelon®), approved in 2000
  • galantamine (Reminyl®), approved in 2001

NMDA receptor antagonists

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Glutamate is one of the major excitatory neurotransmitters in the brain, including brain regions like the hippocampus where NMDA receptors have been implicated in LTP, a form of long-lasting synaptic change associated with memory storage. It has been suggested that inhibitors of excitatory receptors like NMDA receptors might reduce potential glutamatergic excitotoxicity. "Pathologically-activated therapeutics for neuroprotection: mechanism of NMDA receptor block by memantine and S-nitrosylation" by S. A. Lipton in Curr Drug Targets (2007) May;8(5):621-32.

Memantine is an NMDA receptor antagonist that is approved for treatment of Alzheimer disease[6]

Lipid hypothesis

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There are inherited genetic risk factors for Alzheimer disease. The most important genetic risk factor for Alzheimer disease is one common variant of the Apolipoprotein E gene. The link between Apolipoprotein E and Alzheimer disease is not clear, but this association has stimulated research into the role of lipid metabolism in Alzheimer disease. Some data from human subjects suggest that human use of a subclass of HMG-CoA reductase inhibitors can reduce the incidence of Alzheimer disease[7].

Ginkgo biloba

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It has been suggested that herbal supplements such as Ginkgo biloba might have antioxidant, anti-inflammatory and other actions that could limit neurodegenerative cell damage in Alzheimer disease. [8]

A recent review of herbal medicines called for better studies to compare Ginkgo biloba and other herbal remedies to currently used treatments such as cholinesterase inhibitors[9]

Molecular steps

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Long-term

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A peptide that blocks N-cadherin function disrupts long-term memory formation[10].

Beta-catenin has also been shown to play a role in synaptic function[11].

NMDA receptors (NMDAR) are important neurotransmitter receptors involved in synaptic plasticity and memory. It has been shown that NMDAR activity is coupled to control of N-cadherin and beta-catenin levels in synapses[12]

References

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  1. ↑ Online textbook: Studies of Learning and Memory in Humans in Basic Neurochemistry: Molecular, Cellular and Medical Aspects (Sixth Edition).
  2. ↑ 2.0 2.1 The anatomy of amnesia by Jeffrey J. Gold and Larry R. Squire in Learning and Memory (2006) Volume 13 pages 699-710.
  3. ↑ Memory and the Medial Temporal Lobe. The first published information about H.M. was in "Loss of Recent Memory After Bilateral Hippocampal Lesions," by William Beecher Scoville and Brenda Milner in The Journal of Neurology, Neurosurgery and Psychiatry (1957) Volume 20, pages 11–21.
  4. ↑ Use of Hippocampal and Amygdalar Volumes on Magnetic Resonance Imaging to Predict Dementia in Cognitively Intact Elderly People by Tom den Heijer, Mirjam I. Geerlings, Freek E. Hoebeek, Albert Hofman, Peter J. Koudstaal and Monique M. B. Breteler in Arch Gen Psychiatry (2006) Volume 63 pages 57-62.
  5. ↑ Cholinesterase Inhibitors in Mild Cognitive Impairment: A Systematic Review of Randomised Trials by Roberto Raschetti, Emiliano Albanese, Nicola Vanacore, and Marina Maggini in PLoS Medicine (2007) November; 4(11): e338.
  6. ↑ Use of memantine to treat Alzheimer's disease by Serge Gauthier, Nathan Herrmann, Florian Ferreri, and Catherine Agokou in Canadian Medical Association Journal (2006) August 29; 175(5): 501–502.
  7. ↑ Roles of Cholesterol and Lipids in the Etiopathogenesis of Alzheimer's Disease by Leonel Rojo, Marcela K. Sjöberg, Paula Hernández, Cristian Zambrano, and Ricardo B. Maccioni in Journal of Biomedicine Biotechnology (2006): 73976.
  8. ↑ Evidence-Based Research in Complementary and Alternative Medicine III: Treatment of Patients with Alzheimer's Disease by Francesco Chiappelli, Audrey M. Navarro, David R. Moradi, Ercolano Manfrini, and Paolo Prolo in Evidence Based Complement Alternative Medicine (2006) December; 3(4): 411–424.
  9. ↑ The Use of Herbal Medicine in Alzheimer's Disease—A Systematic Review by Leopoldo Luiz dos Santos-Neto, Maria Alice de Vilhena Toledo, Patrícia Medeiros-Souza and Gustavo Almeida de Souza in Evidence Based Complementary and Alternative Medicine (2006) December; 3(4): 441–445.
  10. ↑ N-cadherin regulates cytoskeletally associated IQGAP1/ERK signaling and memory formation by C. Schrick, A. Fischer, D. P. Srivastava, N. C. Tronson, P. Penzes and J. Radulovic in Neuron (2007) Volume 55 pages 786-798.
  11. ↑ beta-Catenin regulates excitatory postsynaptic strength at hippocampal synapses by T. Okuda, L. M. Yu, L. A. Cingolani, R. Kemler and Y. Goda in Proc Natl Acad Sci U S A. (2007) Volume 104 pages 13479-13484.
  12. ↑ Activity-regulated N-cadherin endocytosis by C. Y. Tai, S. P. Mysore SP, C. Chiu and E. M. Schuman in Neuron (2007) Volume 54 pages 771-785.
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External resources

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