Tau Pathology Without Aβ—A Limited PART of Clinical Progression

Landau, Susan; Mormino, Elizabeth C.

doi:10.1001/jamaneurol.2023.1081

Cited by 2 publications

(2 citation statements)

References 24 publications

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“…looking at clinical features in definite PART participants showed that tau was associated with poorer cognitive performance without the presence of amyloid 10 . Correspondingly, findings from a study conducted by Landau & Mormino further indicate that an increase in medial temporal lobe tau, without amyloid, is associated with cognitive decline 34 . The association between tau and lower cognitive performance has been inconsistent with some prior tau PET investigations 35 .…”

Section: Discussionmentioning

confidence: 97%

“… 10 Correspondingly, findings from a study conducted by Landau & Mormino further indicate that an increase in medial temporal lobe tau, without amyloid, is associated with cognitive decline. 34 The association between tau and lower cognitive performance has been inconsistent with some prior tau PET investigations. 35 However, since participants in this study had a more limited tau distribution than the present study it is difficult to compare these results.…”

Section: Discussionmentioning

confidence: 98%

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Significance of a positive tau PET scan with a negative amyloid PET scan

Robinson,

Lee,

Min

et al. 2023

Alzheimer's & Dementia

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INTRODUCTIONThe implications of positive tau positron emission tomography (T) with negative beta amyloid positron emission tomography (A) are not well understood. We investigated cognitive performance in participants who were T+ but A‐.METHODSWe evaluated 98 participants from the Mayo Clinic who were T+ and A‐. Participants were matched 2:1 to A‐ and T‐ cognitively unimpaired (CU) controls. Cognitive test scores were compared between different groups.RESULTSThe A‐T+ group demonstrated lower performance than the A‐T‐ group on the Mini‐Mental Status Exam (MMSE) (p < 0.001), Wechsler Memory Scale‐Revised Logical Memory I (p < 0.001) and Logical Memory II (p < 0.001), Auditory Verbal Learning Test (AVLT) delayed recall (p = 0.004), category fluency (animals p = 0.005; vegetables p = 0.021), Trail Making Test A and B (p < 0.001), and others. There were no significant differences in demographic features or apolipoprotein E (APOE) e4 genotype between CU A‐T+ and CI A‐T+.DISCUSSIONA‐T+ participants show an association with lower cognitive performance.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

Significance of a positive tau PET scan with a negative amyloid PET scan

Robinson,

Lee,

Min

et al. 2023

Alzheimer's & Dementia

View full text Add to dashboard Cite

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Revised criteria for diagnosis and staging of Alzheimer's disease: Alzheimer's Association Workgroup

Jack,

Andrews,

Beach

et al. 2024

Alzheimer's & Dementia

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The National Institute on Aging and the Alzheimer's Association convened three separate work groups in 2011 and single work groups in 2012 and 2018 to create recommendations for the diagnosis and characterization of Alzheimer's disease (AD). The present document updates the 2018 research framework in response to several recent developments. Defining diseases biologically, rather than based on syndromic presentation, has long been standard in many areas of medicine (e.g., oncology), and is becoming a unifying concept common to all neurodegenerative diseases, not just AD. The present document is consistent with this principle. Our intent is to present objective criteria for diagnosis and staging AD, incorporating recent advances in biomarkers, to serve as a bridge between research and clinical care. These criteria are not intended to provide step‐by‐step clinical practice guidelines for clinical workflow or specific treatment protocols, but rather serve as general principles to inform diagnosis and staging of AD that reflect current science.Highlights We define Alzheimer's disease (AD) to be a biological process that begins with the appearance of AD neuropathologic change (ADNPC) while people are asymptomatic. Progression of the neuropathologic burden leads to the later appearance and progression of clinical symptoms. Early‐changing Core 1 biomarkers (amyloid positron emission tomography [PET], approved cerebrospinal fluid biomarkers, and accurate plasma biomarkers [especially phosphorylated tau 217]) map onto either the amyloid beta or AD tauopathy pathway; however, these reflect the presence of ADNPC more generally (i.e., both neuritic plaques and tangles). An abnormal Core 1 biomarker result is sufficient to establish a diagnosis of AD and to inform clinical decision making throughout the disease continuum. Later‐changing Core 2 biomarkers (biofluid and tau PET) can provide prognostic information, and when abnormal, will increase confidence that AD is contributing to symptoms. An integrated biological and clinical staging scheme is described that accommodates the fact that common copathologies, cognitive reserve, and resistance may modify relationships between clinical and biological AD stages.

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Tau Pathology Without Aβ—A Limited PART of Clinical Progression

Cited by 2 publications

References 24 publications

Significance of a positive tau PET scan with a negative amyloid PET scan

Significance of a positive tau PET scan with a negative amyloid PET scan

Revised criteria for diagnosis and staging of Alzheimer's disease: Alzheimer's Association Workgroup

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