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Front Cell Neurosci. 2019 Dec 5;13:538. doi: 10.3389/fncel.2019.00538. eCollection 2019.

Increased Inflammation and Unchanged Density of Synaptic Vesicle Glycoprotein 2A (SV2A) in the Postmortem Frontal Cortex of Alzheimer's Disease Patients.

Author information

1
Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.
2
Translational Neuropsychiatry Unit, Aarhus University, Aarhus, Denmark.
3
Department of Nuclear Medicine and PET-Center, Aarhus University, Aarhus, Denmark.
4
Department of Medical Neuroscience, Dalhousie University, Halifax, NS, Canada.
5
Department of Medicine, Neurology, and Geriatric Medicine, Dalhousie University, Halifax, NS, Canada.

Abstract

Sections from the middle frontal gyrus (Brodmann area 46) of autopsy-confirmed Alzheimer's disease (AD) patients and non-demented subjects were examined for the prevalence of hallmark AD pathology, including amyloid-β (Aβ) plaques, phosphorylated tau (pTau) tangles, neuroinflammation and synaptic loss (n = 7 subjects/group). Dense-core deposits of Aβ were present in all AD patients (7/7) and some non-demented subjects (3/7), as evidenced by 6E10 immunohistochemistry. Levels of Aβ immunoreactivity were higher in AD vs. non-AD cases. For pTau, AT8-positive neurofibrillary tangles and threads were exclusively observed in AD patient tissue. Levels of [3H]PK11195 binding to the translocator protein (TSPO), a marker of inflammatory processes, were elevated in the gray matter of AD patients compared to non-demented subjects. Levels of [3H]UCB-J binding to synaptic vesicle glycoprotein 2A (SV2A), a marker of synaptic density, were not different between groups. In AD patients, pTau immunoreactivity was positively correlated with [3H]PK11195, and negatively correlated with [3H]UCB-J binding levels. No correlation was observed between Aβ immunoreactivity and markers of neuroinflammation or synaptic density. These data demonstrate a close interplay between tau pathology, inflammation and SV2A density in AD, and provide useful information on the ability of neuroimaging biomarkers to diagnose AD dementia.

KEYWORDS:

[3H]PK11195; [3H]UCB-J; amyloid; neuroinflammation; synapses; synaptic vesicle glycoprotein 2A; tau; translocator protein

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