Amyloid and Tau PET Positivity in Progressive Agrammatic Aphasia and Apraxia of Speech.

Alzheimer’s disease amyloid-β protein biomarkers tau protein

Journal

Journal of Alzheimer's disease : JAD
ISSN: 1875-8908
Titre abrégé: J Alzheimers Dis
Pays: Netherlands
ID NLM: 9814863

Informations de publication

Date de publication:
2023
Historique:
pubmed: 26 11 2023
medline: 26 11 2023
entrez: 26 11 2023
Statut: ppublish

Résumé

The agrammatic variant of primary progressive aphasia (PAA), primary progressive apraxia of speech (PPAOS), or a combination of both (AOS-PAA) are neurodegenerative disorders characterized by speech-language impairments and together compose the AOS-PAA spectrum disorders. These patients typically have an underlying 4-repeat tauopathy, although they sometimes show evidence of amyloid-β and tau deposition on PET, suggesting Alzheimer's disease (AD). Given the growing number of pharmacologic treatment options for AD, it is important to better understand the incidence of AD pathology in these patients. This study aimed to evaluate the frequency of amyloid-β and tau positivity in AOS-PAA spectrum disorders. Sixty-five patients with AOS-PAA underwent a clinical speech-language battery and PiB PET and flortaucipir PET imaging. Global PiB PET standardized uptake value ratios (SUVRs) and flortaucipir PET SUVRs from the temporal meta region of interest were compared between patient groups. For 19 patients who had died and undergone autopsy, their PET and pathology findings were also compared. The results showed that although roughly half of the patients are positive for at least one biomarker, their clinical symptoms and biomarker status were not related, suggesting that AD is not the primary cause of their neurodegeneration. All but one patient in the autopsy subset had a Braak stage of IV or less, despite four being positive on tau PET imaging. Inclusion criteria for clinical trials should specify clinical presentation or adjust the evaluation of such treatments to be specific to disease diagnosis beyond the presence of certain imaging biomarkers.

Sections du résumé

BACKGROUND BACKGROUND
The agrammatic variant of primary progressive aphasia (PAA), primary progressive apraxia of speech (PPAOS), or a combination of both (AOS-PAA) are neurodegenerative disorders characterized by speech-language impairments and together compose the AOS-PAA spectrum disorders. These patients typically have an underlying 4-repeat tauopathy, although they sometimes show evidence of amyloid-β and tau deposition on PET, suggesting Alzheimer's disease (AD). Given the growing number of pharmacologic treatment options for AD, it is important to better understand the incidence of AD pathology in these patients.
OBJECTIVE OBJECTIVE
This study aimed to evaluate the frequency of amyloid-β and tau positivity in AOS-PAA spectrum disorders. Sixty-five patients with AOS-PAA underwent a clinical speech-language battery and PiB PET and flortaucipir PET imaging.
METHODS METHODS
Global PiB PET standardized uptake value ratios (SUVRs) and flortaucipir PET SUVRs from the temporal meta region of interest were compared between patient groups. For 19 patients who had died and undergone autopsy, their PET and pathology findings were also compared.
RESULTS RESULTS
The results showed that although roughly half of the patients are positive for at least one biomarker, their clinical symptoms and biomarker status were not related, suggesting that AD is not the primary cause of their neurodegeneration. All but one patient in the autopsy subset had a Braak stage of IV or less, despite four being positive on tau PET imaging.
CONCLUSIONS CONCLUSIONS
Inclusion criteria for clinical trials should specify clinical presentation or adjust the evaluation of such treatments to be specific to disease diagnosis beyond the presence of certain imaging biomarkers.

Identifiants

pubmed: 38007664
pii: JAD230912
doi: 10.3233/JAD-230912
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1759-1765

Auteurs

Katerina A Tetzloff (KA)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Joseph R Duffy (JR)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Heather M Clark (HM)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Nha Trang Thu Pham (NTT)

Department of Radiology, Mayo Clinic, Rochester, MN, USA.

Mary M Machulda (MM)

Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN, USA.

Hugo Botha (H)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Clifford R Jack (CR)

Department of Radiology, Mayo Clinic, Rochester, MN, USA.

Dennis W Dickson (DW)

Department of Radiology, Mayo Clinic, Rochester, MN, USA.

Val J Lowe (VJ)

Department of Radiology, Mayo Clinic, Rochester, MN, USA.

Keith A Josephs (KA)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Jennifer L Whitwell (JL)

Department of Radiology, Mayo Clinic, Rochester, MN, USA.

Rene L Utianski (RL)

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Classifications MeSH