Predementia Stages Of Alzheimer's Disease Research Articles

Mild Cognitive Impairment Is Not a Clinical Entity and Should Not Be Treated

T HERE HAS BEEN GREAT progress in the diagnosis and treatment of Alzheimer disease (AD) and related dementias thanks to the availability of well-validated diagnostic criteria (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV); National Institute of Neurological and Communicative Disorders and Stroke–the Alzheimer’s Disease and Related Disorders Association [NINCDS-ADRDA]); and a large number of randomized clinical trials using cholinesterase inhibitors (AChEIs) and Memantine. Work from specialized neurological clinics suggests that mild cognitive impairment (MCI) is an early stage of AD, and there is a temptation for neurologists to prescribe AChEIs in this population. On the other hand, there is epidemiological evidence that many subjects labeled as having MCI do not worsen over time and may revert to normal cognitive abilities. A diagnosis of MCI as a predementia stage of AD in such individuals would be inaccurate and carry a heavy personal and societal burden. Reversible causes of MCI may be found, such as depression, upper airway obstruction, and a variety of metabolic, nutritional, or sensory impairments. Since MCI does not constitute a homogeneous clinical syndrome, it is inappropriate to propose a specific drug treatment such as AChEIs, but the recognition that MCI is a risk state toward further cognitive decline is clinically relevant, and control of risk factors such as systolic hypertension, hypercholesterolemia, diabetes mellitus, atrial fibrillation, transient ishemic attacks, and strokes may delay progression to dementia.

Aux frontières de l’Alzheimer

Accurately predicting the development of probable Alzheimer's disease (AD) early in the course of the disease would have major implications. Hence, the pre-dementia stage of AD has become a major topic of current research. Amnestic 'mild cognitive impairment' (MCI) has recently emerged as the most convenient avenue to address this Issue, since most of MCI patients will progress to AD, at a rate of 10% to 15% per Year, suggesting that MCI represents the clinical manifestation of incipient AD (Petersen et al., 2001). However, all MCI patients would probably not convert to AD, at least in the near future, so that the Issue of prospective longitudinal studies is to detect specific indices of rapid conversion. In this paper, we focus on longitudinal studies using either neuropsychology, or morphological or functional neuroimaging to find predictive markers allowing to distinguish those MCI patients that rapidly convert to AD from those that do not develop the disease during the follow-up period. Whereas functional neuroimaging, and more specifically FDG-PET, seems particularly accurate to predict AD, the combination of multiple approaches is likely to be a promising avenue.

Tau protein. A potential biological indicator for early detection of Alzheimer disease

In 40 patients with Alzheimer's disease (AD), in 5 patients with non-AD dementia and in 36 cognitively normal controls the concentration of protein tau was determined in the cerebrospinal fluid (CSF). Of the AD patients, 19 were very mildly demented (MMSE score from 25 to 28). Even in these patients, CSF tau was significantly more elevated than in controls. In the non-AD patients protein tau was less increased. Among the AD patients there was no association between CSF tau and severity of cognitive impairment or deficit in cerebral blood flow, determined by SPECT. Our findings suggest that CSF tau may be elevated even at the predementia stage of AD and be useful as a biological marker for the early recognition of the disease.