Recently articles have appeared suggesting that in transgenic mice, vaccination with small parts of beta-amyloid can produce antibodies that prevent formation of amyloid plaques in the young and banishment in older mice. (Mice do not have tangles.) Because vaccines have eliminated or mitigated the effect of smallpox, polio, tuberculosis, and other dread diseases, such news is electrifying. However, disbelief is not long suspended when certain facts are presented. First, the role of plaques and tangles is moot. Second, there are reckoned to be at least 55 kinds of dementia, with Alzheimer's disease (AD) having a major but decreasing proportion as new types are recognized. (Thus some would argue that Lewy body disease constitutes as much as 20% of all dementias.) Third, AD is not well diagnosed in life, being a postmortem diagnosis. Finally, we now recognize that there is a considerable overlap between AD and vascular dementia in terms of etiobgy and presentation. So just what are we vaccinating against? Beyond that of course is the mixed bag of variables involved in AD. Think of age, gender, race, intelligence, education, aluminum, oxidants, cholinesterase, and vascular risk factors. These are but a few.