We read the article by Fischer et al with interest. [1] It has been established that MCI as a syndrome carries a higher
risk of progression to dementia particularly in carriers of the apoE4
genotype. [2] It is still unclear whether the subtype (amnestic
single domain, amnestic plus other domains, non-amnestic) is a prodrome to
different types of dementia. This differentiation is based on neuropsychological profiles rather than clinical or biological
characteristics.
It has been suggested that non-amnestic MCI may be a relatively
specific prodrome of non-AD dementias such as fronto-temporal dementia
(FTD), DLB or VaD. If proven, amnestic MCI should be the sole target for
very early AD (or pre-dementia AD) therapeutic research and eventually
treatment with potential disease-modifying drugs such as tramiprosate,
flurbiprofen or various amyloid monoclonal antibodies can be safely implemented.
Fischer et al demonstrate that nonamnestic MCI
can also lead to AD, and that amnestic MCI can lead to non-AD dementias. [1]
In may be necessary to refine the classification of prodromal dementia states
to include biological measures such as hippocampal volume using MRI and/or
CSF biomarkers such as â-amyloid fragments and tau.
Finally, it should be noted that 21.5% of subjects with MCI reverted
back to normal cognition. The term "MCI" should be clarified; it is a risk state, not a specific
diagnosis. Finally, cholinesterase inhibitors have not been proven to have adequate safety or efficacy ratio in this population.
References
1. Fischer P, Jungwirth S, Zehetmayer S, et al. Conversion from
subtypes of mild cognitive impairment to Alzheimer dementia. Neurology
2007; 68: 288-291.
2. Gauthier S, Reisberg B, Zaudig M et al. Mild cognitive impairment. The Lancet 2006; 367; 1262-1270.
Disclosure: The author reports no conflicts of interest.
The author of the article had the opportunity to respond but declined.