The Human Memory - what it is, how it works and how it can go wrong
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The Human Memory - what it is, how it works and how it can go wrong
INTRODUCTION
TYPES OF MEMORY
MEMORY PROCESSES
MEMORY DISORDERS
MEMORY & THE BRAIN
SOURCES & REFERENCES

Memory Disorders
  Introduction
  Age Associated
  Alcohol
  Alzheimer's Disease
  Amnesia
     Anterograde Amnesia
     Retrograde Amnesia
     Psychogenic Amnesia
     Post-Traumatic Amnesia
  Autism
  Dementia
  HIV
  Huntington's Disease
  Korsakoff's Syndrome
  OCD
  Parkinson's Disease
  Schizophrenia
  Stroke
  Tourette Syndrome


AGE ASSOCIATED MEMORY IMPAIRMENT

??? Did You Know ???
Normal human memory powers peak at the age of 25, after which they start to decline.
At this time, the brain is capable of remembering over 200 bits of information per second, as well as controlling body movements at the same time, far outstripping the performance of any computer.
Age associated memory impairment is a label for the general degradation of memory which results from ageing. It is a natural process, seen in many animals as well as humans, which often begins in our 20s and tends to get noticeably worse as we reach our 50s. While some specific abilities do decline with age, though, overall memory generally remains strong for most people through their 70s.

Episodic memory (our memory of experiences and specific events in time) in particular is impaired in normal ageing. On the other hand, in the absence of specific neurological disorders, implicit or procedural memory typically shows little or no decline with age, short-term memory shows only a little decline, and semantic knowledge, such as vocabulary, actually tends to improve somewhat with age.

Normal ageing is not responsible for causing memory disorders as such, but it is associated with a general decline in cognitive and neural systems, including memory. As people age, the likelihood of cholinergic dysfunction, beta-amyloid deposits, hippocampal neurofibrillary tangles or neuritic plaques in the cortex of the brain increases, so that memory connections can become blocked, memory functions decrease and the likelihood of memory disorders like dementia and Alzheimerís disease increases. Ageing is the single greatest risk factor for neurodegenerative diseases in general.

Recent research has identified a transitional state between the cognitive changes of normal ageing and Alzheimer's disease, known as mild cognitive impairment, where some memory loss occurs, but is not so severe that it interferes with normal daily functioning. More severe memory loss is defined as dementia, of which Alzheimer's is just one common variant. Those who experience mild cognitive impairment are at a significantly higher risk of developing Alzheimerís disease or other types of dementia, especially after events like strokes.

??? Did You Know ???
A recent report by the Society for Neuroscience suggests that infusions of blood from young mice can reverse the memory decline in older mice, and vice versa.
It is not clear just how this effect works.

Although the brain does not change its overall structure or grow whole new batches of neurons over time, the connections between them change during the normal process of learning, as synapses are reinforced and neural cells make more and stronger connections with each other. As we begin to age, however, these connections begin to falter and weaken, in the same way as other biological processes deteriorate and become more fragmented over time, and this begins to affect how easily we can retrieve memories.

In particular, as the brain ages, the white matter which links together different parts of the brain, begins to die off, largely because the blood flow supplied to the brain is not as healthy as in the young, which causes memory to become impaired. Also, the production of the chemical messengers (neurotransmitters) used to carry signals through the brain is also reduced, perhaps by as much as 50% between young adulthood and old age, which impairs our ability to think and perform memory tasks.

The decline theory of forgetting suggests that, essentially, forgetting occurs when the memory is not exercised, or the information in question is not retrieved often enough to re-consolidate memories. This is illustrated by the order in which words tend to be forgotten in old age: proper nouns, which are typically used less often, are usually the first words to go, followed by common nouns, then adjectives, verbs and, lastly, exclamations and interjections.

??? Did You Know ???
A 2011 study for the American Journal of Clinical Nutrition suggests that a diet high in fruit and vegetables, particularly fruits that are high in Vitamin C and anti-oxidants, can help protect against memory loss due to ageing.

One theory for why this happens, at the cellular level, is that ageing causes major cell loss in a tiny region at the front of the brain that leads to a drop in the production of a neurotransmitter called acetylcholine, which is vital to learning and memory. In addition, the brain itself shrinks in size to some extent, and becomes less efficient as we age. In particular, the hippocampus, which is essential to the proper functioning of the processes of memory, loses about 5% of its nerve cells with each passing decade, up to a total loss of 20% by the age of about 80.

There are, however, several other environmental factors which may combine to speed up memory decline, including the inheritance of unhealthy genes, exposure to toxins and poisons, or lifestyle choices like smoking, drinking or bad diet. Physical exercise and mental stimulation can improve mental function in general, and therefore help to slow memory decline, although there is no "magic bullet" solution as some might claim.

It is also becoming apparent that some drugs used to treat other age-related diseases and conditions may have a deleterious effect on memory and hasten the onset of dementia, among them: anti-anxiety drugs (e.g. benzodiazepines); cholesterol-lowering drugs (e.g. statins); anti-depressant drugs (e.g. tricyclics); anti-seizure and anti-convulsant drugs; narcotic painkillers and opioids; Parkinson's drugs (e.g. dopamine agonists); hypertension drugs (e.g. beta-blockers); sleeping aids (e.g. non-benzodiapezine sedatives); incontinence drugs (e.g. anti-cholinergics); first generation antihistamines; etc.

 
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© 2010 Luke Mastin
 

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