The Department of Nuclear Medicine of Jilin University Second Hospital carried out multi-probe PET/CT imaging related to Alzheimer's disease

The Department of Nuclear Medicine routinely conducts multi-probe PET/CT imaging related to Alzheimer's disease [FDG+Aβ and tau protein]. It can help patients to clarify the cause of the disease, assist the clinicians in further formulating treatment and medication plans, and provide an imaging baseline for the evaluation of treatment effects in the future.

What is Alzheimer's disease

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, mental and behavioral abnormalities, and a decline in the ability to function in daily life. Its characteristic pathological changes are the deposition of β-amyloid (Aβ) and the formation of neurofibrillary tangles in the brain. AD is the most common type of dementia in the elderly, seriously affecting the physical and mental health and quality of life of the elderly.

FDG-PET imaging

In AD, cerebral hypometabolism detected using ¹⁸F-FDG-PET is a hallmark of neurodegeneration. It measures regional glucose consumption that is directly related to the local intensity of glutamatergic synaptic and astrocyte activity in the brain. ¹⁸F-FDG-PET assesses the extent and location of hypometabolism, reflecting neuronal dysfunction. Typical FDG-PET findings in AD patients include decreased glucose metabolism in the temporoparietal cortex, anterior cingulate gyrus, and posterior cingulate gyrus. FDG-PET plays an important role in such findings as vision and quantitative perception, which can improve the accuracy of clinical diagnosis of AD and potentially differentiate AD from non-Alzheimer's dementia.

Aβ-PET imaging

β-amyloid protein (Aβ) is the main component of the pathological protein Aβ plaques at the core of Alzheimer's disease, and its abnormal aggregation is closely related to the onset of Alzheimer's disease. Aβ-PET scan can reflect the deposition of Aβ and visualize specific pathological changes in the brain. It has high sensitivity and specificity, and has the advantages of early, non-invasive and accurate diagnosis. It is an important indicator for efficacy monitoring.

Tau PET imaging

In AD, the hyperphosphorylation of tau protein weakens its binding to microtubules, and the hyperphosphorylated tau protein assembles into fibers. Abnormally phosphorylated tau protein leads to the formation of paired helical filaments (PHF) and nerve fiber tangles (NFT). Studies on tau protein imaging in the diagnosis of AD have found that clinical studies of tau protein imaging agents have shown that abnormal deposition of tau protein in the brain has specific manifestations in AD, mainly located in the medial temporal lobe, lateral temporal lobe and parietal lobe. Tau protein PET/CT imaging can quantitatively express the abnormal spatial distribution of tau protein deposition and can assess the severity of AD.

The significance of combined multi-probe PET imaging

FDG-PET imaging can evaluate the degree and location of hypometabolism in AD patients and reflect neuronal dysfunction. Aβ-PET imaging can quantify amyloid deposition in the brain of AD patients; tau-PET imaging can quantify Tau protein tangles in the brain of AD patients. Multi-probe PET/CT imaging can diagnose Alzheimer's disease qualitatively and quantitatively, and can provide objective imaging basis for early diagnosis and differential diagnosis, efficacy monitoring and prognosis evaluation of AD.

Note: 18F-FDG imaging of patients with Alzheimer's disease showed decreased glucose metabolism in the bilateral parietal lobes, Aβ imaging showed Aβ deposition in the bilateral parietal lobes, and Tau imaging showed obvious deposition of tau protein in the bilateral parietal lobes.

AD patients are generally older than 65 years old, otherwise it is early-onset AD. Early-onset AD patients generally progress faster, and early diagnosis and early treatment are crucial to the patient's quality of life. The typical pathological basis of AD is the deposition of amyloid protein outside neuronal cells to form senile plaques and Tau protein tangles inside neuronal cells. The NIA-AA diagnosis and treatment guidelines clearly point out that positive nuclear medicine PET molecular probe Aβ and Tau protein imaging can confirm AD.

Author: Lv Shupeng

First review: Hao Tingting

Final judge: Zhao Yinlong