F-18 ML-104 tau PET imaging in mild cognitive impairment

• Published in: Nuclear medicine communications Vol. 42; no. 8; pp. 914 - 921
• Main Authors: Jaleel, Jasim, Tripathi, Madhavi, Baghel, Vivek, Arunraj, Sreedharan Thankarajan, Kumar, Praveen, Khan, Dikhra, Tripathi, Manjari, Dey, Aprajit Ballav, Bal, Chandrasekhar
• Format: Journal Article
• Language: English
• Published: England 01-08-2021
• Subjects: Aged; Aniline Compounds; Case-Control Studies; Cognitive Dysfunction - diagnostic imaging; Cognitive Dysfunction - metabolism; Female; Humans; Male; Middle Aged; Positron-Emission Tomography - methods; tau Proteins - metabolism
• ISSN: 0143-3636; 1473-5628; 1473-5628
• DOI: 10.1097/MNM.0000000000001415

This study was undertaken to evaluate the tau distribution patterns in patients with amnestic mild cognitive impairment (aMCI) using PET radiotracer F-18 ML-104.
Thirty patients, clinically diagnosed as aMCI [mini mental state evaluation ≥24] in the neurology or geriatric memory clinics, were included in the study. Each aMCI patient underwent F-18 fluorodeoxyglucose and F-18 ML-104 tau PET. Standardized uptake value ratios for cortical gray matter regions were evaluated for F-18 ML-104 tau PET and compared with normal controls and with early Alzheimer's disease (AD) patients (used from a previous study).
aMCI revealed significantly higher standardized uptake value ratios in both medial temporal cortices, precuneus and posterior cingulate cortices in comparison to normal controls and a significantly lesser binding in bilateral medial and lateral temporal, precuneus and posterior cingulate cortices in comparison to early AD. A negative correlation was noted between F-18 fluorodeoxyglucose uptake and F-18 ML-104 retention in the precuneus and posterior cingulate cortices in aMCI, while F-18 ML-104 retention and mini mental state evaluation scores revealed a moderate negative correlation in the posterior cingulate cortices.
We could demonstrate a significant increase in cortical tau deposition in aMCI patients in comparison to normal controls, thus providing in vivo evidence of the underlying pathological process in this subgroup of patients with high probability of conversion to AD.