Background:
Visuospatial dysfunction is one predominant symptom in many atypical Alzheimer’s
disease (AD) patients, however, until now its neural correlates still remain unclear. For the accumulation
of intracellular hyperphosphorylated tau proteins is a major pathogenic factor in neurodegeneration
of AD, the distributional pattern of tau could highlight the affected brain regions associated
with specific cognitive deficits.
Objective:
We investigated the brain regions particularly affected by tau accumulation in patients with
visuospatial dysfunction to explore its neural correlates.
Methods:
Using 18F-AV-1451 tau positron emission tomography (PET), voxel-wise two-sample t-tests
were performed between AD patients with obvious visuospatial dysfunction (VS-AD) and cognitively
normal subjects, AD patients with little-to-no visuospatial dysfunction (non VS-AD) and cognitively
normal subjects, respectively.
Results:
Results showed increased tau accumulations mainly located in occipitoparietal cortex, posterior
cingulate cortex, precuneus, inferior and medial temporal cortex in VS-AD patients, while increased tau
accumulations mainly occurred in the inferior and medial temporal cortex in non VS-AD patients.
Conclusion:
These findings suggested that occipitoparietal cortex, posterior cingulate cortex and precuneus,
which were particularly affected by increased tau accumulation in VS-AD patients, may associate
with visuospatial dysfunction of AD.
Relationship Between Alzheimer Disease-Like Pattern of 18F-FDG and Fasting Plasma Glucose Levels in Cognitively Normal Volunteers
