Think Medications for Dementia Produce No Meaningful Benefit? Don’t Be So Sure

Currently available anti-Alzheimer drugs – donepezil (Aricept), galantamine (Razadyne), rivastigmine (Exelon), and memantine (Namenda) – are not the miracle cures patients hope for, and many clinicians are skeptical, and don’t prescribe them. Consumers nevertheless have heard that these drugs at least “slow it down”, and many accept this as better than nothing.

But do anti-Alzheimer medications “slow it down”? Unfortunately, scientists do not know for sure. Some research demonstrates actions in the brain of anti-Alzheimer drugs that could be helpful, but there has been no proof that these effects interrupt the disease process. Specialists who recommend these medications mostly believe that their benefits are limited to temporary improvement of symptoms, stabilizing their patients’ conditions for a time, before they resume relentlessly losing ground to dementia. What remains unknown is whether treated patients continue to decline at the same rate as before or slower. A new study provides reason to think that anti-Alzheimer drugs actually might slow down patients’ decline.

Last month French researchers published a study of patients with mild cognitive impairment.*  Mild cognitive impairment (you may hear it referred to as mild neurocognitive disorder) is a milder condition not severe enough to be considered a dementia. About half of the time, however, MCI is a preliminary stage of Alzheimer’s disease: such patients gradually get worse and sooner or later develop dementia.

In this French study, patients with MCI were treated for one year: half received donepezil (Aricept) and half placebo. At the beginning of the study, and again at the end of the year, patients had brain MRI scans, and the thickness of their cerebral cortex was measured. The cortex is the outer layer of the brain, where memory and other higher mental abilities reside. As Alzheimer’s disease worsens the cerebral cortex gets thinner and thinner. Researchers compared the amount of thinning in those who received donepezil with those who did not. The good news is that the patients treated with donepezil had much less cortical thinning than those who received placebo. In some brain areas, the cortex even got thicker! This finding suggests that treatment with anti-Alzheimer medications may actually slow down the rate at which patients decline

While encouraging, this study has many weaknesses, so it is far from a slam-dunk proof of anything. But it does provide another bit of evidence that anti-Alzheimer drugs may not be as worthless as many think. If these drugs do slow the rate of decline, the benefit might not be apparent early in treatment, but would be more and more obvious, and meaningful, as time goes on because patients stay further and further ahead of where they would have been without treatment. This is a different way to think about medical treatment, but nonetheless a meaningful one, especially for Alzheimer patients and their families.

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