Tuesday, 26 June 2012

Alzheimer’s Disease

  What is Alzheimer’s  Disease?
 INTRODUCTION:
Alzheimer's disease is a brain disease of unknown cause that leads to dementia. Most patients with Alzheimer's disease are over 65 years of age. 
The most common cause of dementia is a  primary cerebral disorder called Alzeimer’s disease or primary dementia of the Alzeimers type, which was first described in 1907 by a neuropsychiatrst, alois  alzeimers .Alzeimers disease is recognized as a syndrome of clinical features characterized by a decline of memory and other cognitive functions in comparison with  the patient previous level of  function.
Alzeimers disease  has an insidious onset, is progressive and is differentiated by the exclusion of other disease that would account for the cognitive areas such as languge use ,visual-spatial perception ,the ability to learn ,solve problems, think abstractly and make judgements are also affected.
EPIDEMIOLOGY:
 Alzeimers disease is responsible for about 55% of cases of dementia and afflicts approximately 2 to 4 million people in the US. A recent study found that 10.3% of the population over 65 has Alzeimers disease. The prevalence increases with age.
ETIOLOGY
Althohgh the dementia syndrome may  be caused by over 60 disorders ,most cases are due to Alzeimers disease followed by multi infarct dementia or a combination of the two.
     Alzeimers disease is thought to be correlated with diminished neuron function and a decrease function and a decrease in neurotransmitters. The major biochemical abnormality observed in alzeimers disease is a 40 to 90% decrease in the enzyme  choline acetyl transferase in the cerebral  cortex  and hippocampus.
 The defeciency of this enzyme causes decreases synthesis of acetyl choline  in the brain . The loss of acetyl-transferase in the brain  appears to begin  within the first  year of onset of the symptoms of dementia, and there seems to be a strong correlation between the degree of enzyme reduction and the decline of mental status scores.
Trials with precursors of acetylcholine such as choline or lecithin have predictably not demonstrated  improvement  in mental  status. Since alzeimers disease patients lack acetyl transferase and are unable to convert the precursors  to acetylcholine. 
On the other hand ,drugs such as physostigmine ,which blocks  acetyl transferase and therefore  decrease  the catabolism  of  acetylcholine have had limited success. This type of  drug would  only be effective when acetylcholine  is still being formed by the remaining cholinergic neurons.  
              
 Acetylcholine is the primary neurotransmitter deficit associated with Alzeimers disease .but other neurotransmitters have been implicated. For example, somatostatin is often deficient in patients with alzeimers disease, as the number of somatostatin receptors.
There is also a study that reports a decrease in corticotrophin –releasing factor. Variable losses in the amount  of norepinephrine, the biosynthetic enzyme dopamine  ß-hydroxylase, and serotonin cells have been shown with alzeimers disease.

No comments:

Post a Comment