A number of factors such as non-steroidal anti-inflammatory drugs, hormone replacement therapy, and the antioxidant vitamin E, might be of some use in strategies to prevent AD. Prevention could be primary before any signs of the disease or secondary after some manifestation of the process. Primary preventive measures would have to be directed at either the entire population or to groups at risk (identified by family history or genotype, for example), and therefore would have to be entirely benign and almost cost-free to be acceptable. Secondary prevention, possibly in those with memory impairments not amounting to dementia (minimal cognitive impairment), is a more realistic prospect rendering the determination of the very earliest signs of disease or evidence of a prodromal state a high priority. A biological marker for AD would have immense utility in both clinical practice and in clinical trials. Markers suggested have included platelet membrane fluidity and measurement of amyloid, apoE, and tau in cerebrospinal fluid, as well as genetic markers. (82) Of these only cerebrospinal fluid tau appears to have any possible value as a biomarker.
Tertiary prevention or disease modification refers to treatments to arrest or slow down the disease process after it has become clinically evident. Some evidence exists that drugs already available might have a disease-modifying effect, and other compounds designed to reduce amyloid formation or aggregation or tau phosphorylation are in development. Other approaches have been developed to reduce the inflammatory component of pathogenesis, or to enhance function and provide support for the remaining neurones using nerve growth factor. This latter promising approach is made problematic by the fact that oral or parenteral administration of a peptide would result in its rapid degradation.
Given that AD is a chronically deteriorating condition, determining efficacy of disease modification is difficult. Two approaches have been suggested. (83) The randomized start trial assigns patients to drug or placebo at random, and at some predetermined point those on placebo are switched to treatment. If the treatment is symptomatic only it would be expected that on switching to treatment these individuals would 'catch-up' with those treated from the outset. However, if the treatment has slowed the disease, those treated from the outset would remain relatively improved compared to the switched group. The randomized withdrawal trial is a reverse of this, with patients withdrawn from active treatment failing to fall to the placebo group results if the compound had affected the disease process.
Was this article helpful?
Everything you wanted to know about. How To Cure Tennis Elbow. Are you an athlete who suffers from tennis elbow? Contrary to popular opinion, most people who suffer from tennis elbow do not even play tennis. They get this condition, which is a torn tendon in the elbow, from the strain of using the same motions with the arm, repeatedly. If you have tennis elbow, you understand how the pain can disrupt your day.