Alzheimer's Disease
Genetics, Prevention,
and Treatment
Johns Hopkins Neuropsychiatry and Memory Group
| Risk factors for AD | |
| ! Head injury | |
| ! Age | |
| ! Affected relatives | |
| $ risk is ~19% in first-degree | |
| $ 10% in second | |
| $ 5% in controls | |
| Two Kinds of AD? | |
| ! Familial | |
| $ 10% of all cases | |
| $ early onset 40-50's | |
| $ 50% risk of inheritance | |
| ! Sporadic | |
| $ 90% of cases | |
| $ late onset 70-80's | |
| One kind of AD? | |
| ! Late onset makes AD look less genetic | |
| $ death from competing causes | |
| ! Theoretical 90 year risk is 50% | |
| $ especially if rigorous criteria are used | |
| ! Actual risk is about 19% for relatives | |
| Many kinds of AD? | |
| ! 3 early onset genes | |
| $ chromosome 21 APP | |
| $ chromosome 14 pre-senilin 1 | |
| $ chomosome 1 pre-senilin 2 | |
| ! One late onset gene | |
| $ chromosome 19 APOE | |
| APOE | |
| ! 3 alleles: e2, e3, e4 | |
| ! Most people have e3/e3 | |
| ! Risk doubles with one e4, xl5 with 2 e4 | |
| ! e2 may be protective | |
| ! APOE is commonest known genetic cause | |
| Environmental Factors |
| ! Known genetic causes only account for ~50% |
| ! Identical twins are only 58% concordant |
| ! Many people with e4/e4 do not get AD |
| ! May be provocative and preventative factors. |
| Purpose of Prevention | |
| ! Prevent disease | |
| ! Delay onset of disease | |
| $ with late onset often the same | |
| $ 5 year delay could reduce harm by 50% | |
| ! Don't confuse prevention and treatment | |
| Prevention- NSAIDS | |
| ! Several restrospective studies | |
| ! Twin study looks at discordant pairs | |
| $ the non-AD twins took more AI medicine | |
| ! NSAIDS may delay the onset of AD | |
| ! Prospective data would be more convincing | |
| Prevention - Estrogen |
| ! Retrospective studies mostly |
| ! One suggestive treatment trial |
| ! Better prevention and treatment trials are on |
| ! There are other reasons to take estrogens |
| Treatment- Acetylcholinesterase Inhibitors | |
| ! Increase activity in remaining neurons | |
| $ improves performance | |
| $ probably does not change final results | |
| ! Tacrine-Cognex | |
| $ effective but difficult to use | |
| ! Donepezil-Aricept | |
| ! More in the works | |
| Treatment-Vitamin E | |
| ! A single study of Vit E and selegiline | |
| ! Prospective double-blind study | |
| ! Randomization failed | |
| $ placebo group started out higher | |
| $ no significant differences seen | |
| ! Effect only appears if this is corrected for | |
| ! Vit E and selegine may slow progression | |
| Should I be tested? | |
| ! Limitations | |
| $ most people will be negative | |
| $ positives will not all get AD | |
| $ lack of interventions | |
| $ psychosocial consequences | |
| ! Uses | |
| $ diagnostic dilemmas | |
| $ very strong family history | |
| Should I take medicine? | |
| ! Strong scientific support is lacking | |
| ! The risk may be low | |
| ! The interventions are not harmless | |
| $ cost, side effects, confusion | |
| ! Estrogen, aspirin for other indications | |
| Hope | |
| ! Need to understand genetics/environment | |
| $ make better predictions | |
| $ intervene in the process | |
| ! Test promising treatments thoroughly | |
| $ find out how best to apply them | |
| $ prevent harm from adverse effects | |
| ! The future looks good | |