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Related Experiment Videos

Multireceptor fingerprints in progressive supranuclear palsy.

Wang Zheng Chiu1, Laura Donker Kaat1, Agnita J W Boon1

  • 1Department of Neurology, Erasmus Medical Centre, Rotterdam, The Netherlands.

Alzheimer'S Research & Therapy
|April 18, 2017
PubMed
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Neurotransmitter receptor changes in the brain, particularly in the midcingulate cortex, distinguish progressive supranuclear palsy (PSP) subtypes. Kainate and adenosine A1 receptors are altered in PSP, suggesting new treatment targets.

Area of Science:

  • Neuroscience
  • Neurochemistry
  • Neuropathology

Background:

  • Progressive supranuclear palsy (PSP) can present with frontal lobe symptoms, including cognitive and behavioral changes, distinct from classical forms.
  • The midcingulate cortex, crucial for executive functions and attention, shows consistent impairment in PSP imaging studies.
  • Understanding neurotransmitter alterations is key to PSP pathophysiology and its clinical variations.

Purpose of the Study:

  • To investigate neurotransmission alterations in the brain of patients with PSP.
  • To determine the significance of these alterations for distinct clinical PSP subgroups.
  • To explore the role of nondopaminergic systems in PSP.

Main Methods:

  • In vitro receptor autoradiography was employed to quantify densities of 20 different receptors.
Keywords:
Caudate nucleusFrontal presentationMidcingulate cortexNeurotransmitter receptorsProgressive supranuclear palsy

Related Experiment Videos

  • Receptor densities were measured in the caudate nucleus and midcingulate area 24' of PSP patients (n=16) and controls (n=14).
  • Clinical parameters, including frontal presentation and tau pathology severity, were considered.

    • Main Results:

    • Significant increases in gamma-aminobutyric acid type B, peripheral benzodiazepine, serotonin type 2, and N-methyl-D-aspartate receptors were observed in the midcingulate cortex of PSP patients.
    • Kainate and nicotinic cholinergic receptor densities were lower, while adenosine type 1 (A1) receptors were higher in the caudate nucleus of PSP patients.
    • Receptor profiles differentiated PSP subgroups based on clinical presentation and tau pathology.

    Conclusions:

    • Kainate and adenosine A1 receptors are demonstrably altered in PSP, with distinct neurochemical profiles for clinical subgroups.
    • The midcingulate cortex exhibits numerous receptor alterations, indicating its potential central role in PSP.
    • Nondopaminergic systems are implicated in PSP pathophysiology, suggesting novel therapeutic avenues.