The drug is thought to block the excitotoxic effects of abnormal transmission mediated by glutamate, while at the same time allowing for the transmissions associated with normal cell function.
Although no long-term, prospective studies have confirmed the data, some observational investigations have shown evidence that hormone replacement therapy slows down the onset of Alzheimer's disease in women (Growdon, The Search, 2002). Observational studies have also suggested that non-steroidal anti-inflammatories such as ibuprofen and naproxen have a protective effect against Alzheimer's disease, and at least three studies have shown that statins, cholesterol-lowering drugs, also lower the risk of getting the disease.
The goal of research into Alzheimer's disease is to prevent the loss of synapses and neurons in the areas of the brain responsible for memory and cognition (Growdon, The Search 2002). Acetylcholinesterase inhibitors currently used to treat the cognitive symptoms of Alzheimer's disease temporarily compensate for the loss of nerve cells, but don't treat the underlying cause. Antiamyloid drugs and antioxidants are two promising strategies currently being explored. These drugs are hoped to target the cause of the central loss of synapses and neurons. Antiamyloid drugs would block the formation of beta-amyloid, the substance of amyloid plaques, which may be responsible for initiating the events leading to Alzheimer's disease, and believed to be toxic to neurons. In the production of beta-amylase, an enzyme called alpha-secretase cuts the protein in half into nontoxic fragments. If there is overactivation of two other enzymes, beta-secretase and gamma-secretase, a shorter, stickier protein, beta-amyloid, is formed. Current research is trying to develop drugs which either stimulate alpha-secretase, or inhibit beta- and gamma-secretase.
Antioxidants could reduce the damage to neurons from free radicals (Growdon, ...
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