Enzyme once thought harmful to Alzheimers patients now appears key to future...( March 12 2002 -- Bethesda MD -- The f...)

March 12, 2002 -- Bethesda, MD -- The four million Americans who have been diagnosed with Alzheimers disease (AD) experience symptoms which include progressive mental deterioration, confusion, a loss of memory and an inability to calculate the simplest of numbers. This may be due to the fact that people with Alzheimer's have fewer brain cells and less of some important neurotransmitters than people without the disease.

The Importance of Galanin
Previous research has established that a substance called galanin is associated with learning and memory and is involved in brain function, and disorders such as epilepsy. When a nerve is cut or injured, the neuron produces extra galanin, possibly to repair or modulate the damage. The production of galanin may be one way that the body tries to repair nerve damage. Unfortunately, accepted literature states when the onset of AD occurs, galanin hyperinnervation (excessive supply) of nerve cells that employ acetylcholine as their neurotransmitter in the basal forebrain of AD patients occurs and depresses acetylcholine release and its inhibitory actions at other central nervous system sites.

Background
The majority of the scientific community believes this action is detrimental. This is due to a finding that AD wipes out many of the cholinergic neurons of the hippocampus; those that survive in the nucleus show elevated expression of galanin. However, a new study suggests that by virtue of its excitatory actions on cholinergic neurons, galanin may in fact play a compensatory role by enhancing the release of acetylcholine from remaining cholinergic basal forebrain neurons. This action might serve to delay the progression of Alzheimer's disease linked to a reduction in central cholinergic tone. This raises the possibility that induction of galanin by nerve growth factor may have a neuroprotective role.

The Study
To examine this theory, an investigation of the mechanism of action of this
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
14-Mar-2002

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