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Dement Neuropsychol. 2016 Apr-Jun;10(2):79-90. doi: 10.1590/S1980-5764-2016DN1002003.

Imaging Alzheimer's disease pathophysiology with PET.

Author information

1
Translational Neuroimaging Laboratory (TNL), McGill Center for Studies in Aging (MCSA), Douglas Mental Health Research Institute, Montreal, Canada.
2
Alzheimer's Disease Research Unit, MCSA, Douglas Mental Health Research Institute, Montreal, Canada.
3
Brain Institute of Rio Grande do Sul, Pontifical Catholic University of Rio Grande do Sul (PUCRS), Porto Alegre RS, Brazil.
4
Department of Biochemistry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre RS, Brazil.
5
Department NVS, Centre for Alzheimer Research, Division of Translational Alzheimer Neurobiology, Karolinska Institutet, Stockholm, Sweden.

Abstract

in English, Portuguese

Alzheimer's disease (AD) has been reconceptualised as a dynamic pathophysiological process characterized by preclinical, mild cognitive impairment (MCI), and dementia stages. Positron emission tomography (PET) associated with various molecular imaging agents reveals numerous aspects of dementia pathophysiology, such as brain amyloidosis, tau accumulation, neuroreceptor changes, metabolism abnormalities and neuroinflammation in dementia patients. In the context of a growing shift toward presymptomatic early diagnosis and disease-modifying interventions, PET molecular imaging agents provide an unprecedented means of quantifying the AD pathophysiological process, monitoring disease progression, ascertaining whether therapies engage their respective brain molecular targets, as well as quantifying pharmacological responses. In the present study, we highlight the most important contributions of PET in describing brain molecular abnormalities in AD.

KEYWORDS:

Alzheimer's disease; amyloid imaging; neurodegeneration; neuroinflammation; positron emission tomography; tau

Conflict of interest statement

Disclosure: The authors report no conflicts of interest.

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