Need for an Update for the Guideline for the Management of Mild Cognitive Impairment

Abstract

Attention is being paid to diagnosis and treatment of mild cognitive impairment (MCI) because early diagnosis and preventive management can slow down the progression of Alzheimer's disease. In particular, in the present era, the use of biomarkers for predicting conversion into dementia is permitted in medical practice. Therefore, authors aimed to propose additional considerations when updating guidelines for the management of MCI, including predictable biomarkers, revising treatment option after additional clinical trials for cholinesterase inhibitors, and detailed regimes for lifestyle interventions. After reviewing 3 patients with MCI by detailed evaluation, we realized that cholinesterase inhibitors were not recommended. In addition, regular exercise and cognitive training were only possible recommendations for patients according to current guidelines, although all 3 patients had evidence of β-amyloid accumulation and related neurodegeneration. Furthermore, caregivers for all 3 patients were worried whether patients could keep doing regular exercise and cognitive training by themselves and asked about the economic training system which monitors patients so that they can keep training. Therefore, we propose that guidelines for managing MCI need to be updated in the present era when the use of biomarkers for predicting conversion into dementia is permitted in medical practice.

Keywords: Amyloid; Cholinesterase Inhibitors; Guideline; Mild Cognitive Impairment.

Fig. 1. Neuroimaging of Patient 1. Brain MRI showed (A) minimal global brain atrophy, hippocampal atrophy score of 1 on the right and 2 on the left based on the Scheltens’ scale and grade 1 periventricular and grade 1 deep white matter hyperintensities based on the Fazekas scale. F-18 Flutemetamol positron emission tomography computed tomography showed (B) abnormal accumulation of β-amyloid plaque in mainly bilateral frontal lobes, posterior cingulate gyri, precuneus, and left lateral temporal lobe.

Fig. 2. Neuroimaging of Patient 2. Brain magnetic resonance imaging showed (A) left temporal atrophy, hippocampal atrophy score of 0 on the right and 1 on the left based on the Scheltens’ scale and grade 0 periventricular and grade 1 deep white matter hyperintensities based on the Fazekas scale. F-18 Flutemetamol positron emission tomography computed tomography showed (B) abnormal extensive accumulation of β-amyloid plaque in the brain, including the frontal, temporoparietal cortex, and striatum. Subsequent 18F FP-CIT positron emission tomography showed (C) abnormal decreased FP-CIT uptakes in both basal ganglia on delayed phase.

Fig. 3. Neuroimaging of Patient 3. Brain magnetic resonance imaging (A) showed left frontoparietal atrophy, hippocampal atrophy score of 1 on the right and 2 on the left based on the Scheltens’ scale and grade 0 periventricular and grade 1 deep white matter hyperintensities based on the Fazekas scale. F-18 Flutemetamol positron emission tomography computed tomography showed (B) abnormal accumulation of β-amyloid plaque in the frontal, temporoparietal cortex, and striatum. However, 18F FP-CIT positron emission tomography showed (C) normal FP-CIT uptakes in both basal ganglia on delayed phase.