The Alzheimer’s Association International Conference met in Paris in August, 2011. This is an annual meeting that brings out all of the latest research findings.

The first results from the Dominant Inherited Alzheimer’s disease study indicated that that there are measurable changes in cognition, biochemistry, and imaging up to 20 years before symptoms appear. These results are based on studies of high risk individuals who are carriers of a mutant gene that induces early onset Alzheimer’s disease that may develop as early as the 30s and 40s. These findings again confirm that Alzheimer’s disease comes on over the course of decades and that treatment approaches must be proactive. If you wait for symptoms, you lose your advantage.

New research suggests that traumatic brain injury doubles the risk of dementia. These findings are based on a retrospective study of older (55 years or older) veterans. Another related finding was that 35 % of retired NFL players who sustain repetitive head traumas with an average age of 61 had cognitive impairment. This rate far exceeds the rate in the general population (there is an estimated 10% prevalence in those over 65). The relationship between traumatic brain injury and dementia remains controversial as some studies find an association and some don’t (as is true of most areas of science). But what is clear is that those who have sustained head injuries should be followed very carefully as they age for changes in cognitive skills.

Falls in older persons who appear physically and cognitively healthy may be a sign of early Alzheimer’s disease (or other neurological conditions). Progressive neurological disorders don’t always appear at first as cognitive decline. A history of recent falls should be assessed and, if there are falls, a thorough cognitive evaluation should also be conducted.

One headline reads “Modifying Risk Factors May Prevent Alzheimer’s Disease.” The risk factors are smoking, physical inactivity, midlife obesity, midlife hypertension, depression, diabetes, and cognitive inactivity. These factors are not new to those who follow information for “preventing” cognitive decline. The problem is with the word prevention. These factors are correlated with cognitive decline as we age but they don’t cause the decline. There are a number of excellent reasons to attend to these risk factors (e.g., improve overall health and quality of life, reduce medical expenses, and better manage heart disease and cancer) but there is, as yet no evidence that attending to these factor prevents Alzheimer’s disease.

Current beliefs point toward the slowing of brain processes as causing progressive decline in diseases such as Alzheimer’s disease. Preliminary results suggested that this may not be true. Low doses (lower than is used for treating seizures) of Keppra (levetiracetam) slowed the progression of mild cognitive impairment and improved memory. These findings suggest that it is increased activity that may speed progression and that slowing neuroactivity may help slow progression. An interesting new direction to pursue.

Finally, the emphasis in clinical trials has been on drugs that lower amyloids in the brain. These trails have used either immunotherapy or enzymes that remove amyloids. The new finding is that agents that remove amyloids produce edema and microhemorrhages in neurons. This is clearly an adverse effect of amyloid-lowering treatments and may contribute to further neuronal damage. The jury is still out, but I sense a need for caution in moving forward with these classes of drugs.