Biological Causes of Memory Loss

Biological Causes of Memory Loss
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"The true art of memory is the art of attention," said the 18th century British poet Samuel Johnson. The ability to pay attention is indeed a great promoter of one kind of memory, known as "working memory." According to a classic theory proposed by the American psychologist George Miller, working memory, which is located in the prefrontal cortex, can keep up to nine items of information active for cognitive manipulation. Other kinds of memory depend less on attention--such as storage-based short-term memory located in the hippocampus in the brain's temporal lobe and long-term memory located in the cerebral cortex in the brain's outer layer. Besides these memory centers, the brain contains centers for procedural, or routine-based "know-how," memory residing in the striatum and the cerebellum, sometimes referred to as "the little brain."

GABA Pathway

The brain's main depressant neurotransmitter GABA regulates how easily we form new neural connections when presented with new sensory information. It has been known for some time that the connections between neurons in the hippocampus, the brain's main memory center, vary significantly in strength. The variation in strength, however, turns out to correlate with the ability to form new memories, reports a Tel Aviv research team in the August 2010 issue of "Neuron." The researchers found that GABA weakens synaptic connections between neurons in the hippocampus, allowing for new memories to form. Impairments to the GABA pathway or an increase in chemicals that strengthen synaptic connections are thus significant predictors of memory loss. Frequent use of alcohol and benzodiazepines as well as epilepsy, psychotic and neurotic disorders such as bipolar disorder and major depression can impair the GABA pathway. Dementia causes a strengthening of synaptic connections through plaque formations.

Dismantled Neural Connections

Memory loss associated with Alzheimer's disease, schizophrenia, viral and bacterial infections and strokes occurs when neural connections in the hippocampus are dismantled, reports a research team in the January, 2010 issue of "BMC Genomics." A dysfunction of the protein tau, which form microtubule bridges in neurons, is a key player in the dismantling process. When tau doesn't work optimally, the synaptic connections between neurons are lost.

A couple of years earlier a different research team led by University of Sunderland medical researcher Abdel Ennaceur found that skull exposure to infrared light for about 10 minutes a day can rebuild the lost connections. They hit on the idea after studying how infrared light can be used to prevent herpes outbreaks by strengthening the body's immune system.

Sleep Deprivation and Visual Impairment

It has been known for some time that depriving biological organisms of sleep can cause short-term memory loss. Researchers used to believe that sleep deprivation somehow interfered with the storage of information in the hippocampus. But, as a matter of fact, the interference occurs at a lower level of information processing, reports a Singapore research team in the May, 2007 issue of "Proceedings of the National Academy of Sciences." People who are sleep deprived have difficulties attending to visual stimuli, and in some cases the visual system does not fully process seen stimuli. This hinders storage of information in working memory and the hippocampus.

Attention Deficit Hyperactivity Disorder

In 2009, 4.4 million children and adolescents were diagnosed with attention deficit hyperactivity disorder, or ADHD, according to reports released by the National Center for Disease Control and Prevention. ADHD gives rise to frequent malfunction of storage-based short-term memory and working memory. However, the dysfunction is not consistent, reports a U.C. Davis research team in the February 2009 issue of "Child Neuropsychology." A child diagnosed with ADHD may fare as well as an average, normal child on memory tasks on good days but significantly worse on bad, or "hyperactive," days, the scientists found.

References

  • "Neuron"; Basal GABA Regulates GABABR Conformation and Release Probability at Single Hippocampal Synapses; Laviv, et al.; August 2010
  • "BMC Genomics"; High-content siRNA screening of the kinome identifies kinases involved in Alzheimer's disease-related tau hyperphosphorylation; Azorsa, et al.; January 2010
  • MediNewsDirect!: Infrared Radiation Therapy May Help in Reversing Alzheimer Disease
  • "PNAS"; Functional neuroimaging and behavioral correlates of capacity decline in visual short-term memory after sleep deprivation; Chee and Chuah; May 2007

Article reviewed by Julie Mendenhall Last updated on: Aug 3, 2010

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