Τίτλος:
SPECT and PET imaging in Alzheimer’s disease
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia. Beta-amyloid (Aβ) deposition and neurofibrillary tangles (NFTs) of abnormal hyperphosphorylated tau protein are the pathological hallmarks of the disease, accompanied by other pathological processes such as microglia activation. Functional and molecular nuclear medicine imaging with single-photon emission computed tomography (SPECT) and positron emission tomography (PET) techniques provides valuable information about the underlying pathological processes, many years before the appearance of clinical symptoms. Nuclear neuroimaging in AD has made great progress in the past two decades and has extended beyond the traditional role of brain perfusion and glucose metabolism evaluation. Intense efforts in radiopharmaceuticals research have led to the development of various probes able to detect Aβ deposits, tau protein accumulation, microglia activation and neuroinflammation. As a result, SPECT and PET have proposed to serve as biomarkers in recently revised diagnostic clinical criteria for the early diagnosis of AD and the prediction of progression to AD in mild cognitive impairment (MCI) subjects. © 2018, The Japanese Society of Nuclear Medicine.
Συγγραφείς:
Valotassiou, V.
Malamitsi, J.
Papatriantafyllou, J.
Dardiotis, E.
Tsougos, I.
Psimadas, D.
Alexiou, S.
Hadjigeorgiou, G.
Georgoulias, P.
Περιοδικό:
Annals of Nuclear Medicine
Λέξεις-κλειδιά:
amyloid beta protein; tau protein; tau protein, Alzheimer disease; brain perfusion; early diagnosis; glucose metabolism; human; microglia; mild cognitive impairment; nervous system inflammation; neuroimaging; positron emission tomography; priority journal; Review; single photon emission computed tomography; Alzheimer disease; brain; diagnostic imaging; metabolism; pathophysiology; positron emission tomography; procedures; single photon emission computed tomography; vascularization, Alzheimer Disease; Brain; Humans; Positron-Emission Tomography; tau Proteins; Tomography, Emission-Computed, Single-Photon
DOI:
10.1007/s12149-018-1292-6
