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Nutrition in Neurodegenerative Disorders and Cognitive Impairment
Published in David Heber, Zhaoping Li, Primary Care Nutrition, 2017
Alzheimer’s dementia presents with difficulty remembering recent conversations, names, or events. This is often an early clinical symptom. Apathy and depression are also often early symptoms. Later symptoms include impaired communication, poor judgment, disorientation, confusion, behavior changes, and difficulty speaking, swallowing, and walking. Revised criteria and guidelines for diagnosing Alzheimer’s were published in 2011 and affirmed in 2013 (American Psychiatric Association 2013), recommending that Alzheimer’s be considered a slowly progressive brain disease that begins well before symptoms emerge. Abnormalities are deposits of the protein fragment β-amyloid, also known as plaques. Whether these are the key causative factor remains in question, since there are documented cases of amyloid deposits detected by Pittsburgh compound B (PiB)–positron emission tomography (PET) imaging in individuals with normal cognition (Snitz et al. 2015). There are also twisted strands of the protein tau, also called tau tangles, as well as evidence of nerve cell damage and death in the brain. These latter changes would be consistent with inflammation being the primary driver of AD, and this is consistent with what is known about the risk factors, including those that could be impacted by nutrition. A recent study suggested that greater amounts of amyloid at baseline in a prospective study were associated with more rapid progression of AD (Petersen et al. 2016). However, the jury is still out on whether amyloid is the key pathogenic factor or a bystander to an inflammatory process.
Armand
Published in Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner, The Integrated Nervous System, 2017
Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner
The clinical diagnostic criteria detailed in the NCDS-ADRDA guidelines and DSM-V combined with neuroimaging techniques such as CT scan, MRI scan and positron emission tomographic (PET) scans can improve diagnostic certainty. PET scanning of the brain for dementia uses a radionuclide analogue of amyloid called the carbon-11 labelled Pittsburgh compound B to determine the location and degree of disposition of amyloid protein in a given patient’s brain. PET scanning is not readily available in daily clinical practice, and the sensitivity and specificity of the test has not been found to be helpful in early cases of cognitive impairment to predict the future severity of the disease.
Alzheimer's Disease
Published in Marc E. Agronin, Alzheimer's Disease and Other Dementias, 2014
A newer diagnostic approach is to use PET tracers that bind to beta-amyloid plaques in the brain to reveal the relative pathologic load. Early developed compounds include Pittsburgh Compound B or PIB and 18F-FDDNP (Morris et al., 2009). Newer compounds include florbetapir, flutemetamol, and florbetaben, all of which utilize the isotope fluorine 18 with a half-life of 100 minutes—compared to PIB, which uses carbon 11 with a half-life of only 20 minutes (Vallabhajosula, 2011). Florbetapir and flutemetamol are currently on the market and can be used in individuals with known or suspected AD to confirm the presence of beta-amyloid plaques (Wood et al., 2010).
The flutemetamol analogue cyano-flutemetamol detects myocardial AL and ATTR amyloid deposits: a post-mortem histofluorescence analysis
Published in Amyloid, 2023
Eric E. Abrahamson, Robert F. Padera, Julie Davies, Gill Farrar, Victor L. Villemagne, Sharmila Dorbala, Milos D. Ikonomovic
Multiple studies have indicated that PET radiopharmaceuticals [11C]Pittsburgh compound B [22–32], [18F]florbetapir [33–39], [18F]florbetaben [40–44] and [18F]flutemetamol [45–48], typically used to image brain amyloid-β amyloidosis, are retained by cardiac amyloid and have diagnostic value in both AL and ATTR cardiac amyloidosis. However, some studies using these tracers in subjects with cardiac amyloidosis reported false negative results [45]. Whether variation in diagnostic accuracy is related to differences in imaging protocols or is influenced by radioligand binding characteristics to AL/ATTR amyloid is not well understood. While the binding characteristics of amyloid PET radiopharmaceuticals to amyloid-β fibrils has been studied extensively in autopsy brain tissue samples from subjects with brain amyloidosis due to Alzheimer’s disease [49], with the exception of an autoradiography study with [18F]florbetapir [50], the binding characteristics of [18F]flutemetamol and [11C]Pittsburgh compound B to cardiac amyloid deposits remain to be studied.
Non-invasive detection and differentiation of cardiac amyloidosis using 99mTc-pyrophosphate scintigraphy and 11C-Pittsburgh compound B PET imaging
Published in Amyloid, 2020
Ken Takasone, Nagaaki Katoh, Yusuke Takahashi, Ryuta Abe, Naoki Ezawa, Tsuneaki Yoshinaga, Shin Yanagisawa, Masahide Yazaki, Kazuhiro Oguchi, Jun Koyama, Yoshiki Sekijima
Although endomyocardial biopsy is needed for histopathological diagnosis of cardiac amyloidosis [13], this technique is not applicable in all patients due to its relatively high invasiveness and requirement for specific operator skills. Therefore, non-invasive methods to detect cardiac amyloidosis and determine its amyloid subtype are required. Recently, the value of radionuclide molecular imaging for the diagnosis of cardiac amyloidosis has been reported. Technetium-99m (99mTc)-3,3-diphosphono-1,2-propanedicarboxylic acid (DPD), 99mTc-hydroxymethylene diphosphonate (HMDP), and 99mTc-pyrophosphate (PYP) were originally developed as bone-seeking tracers, but are now also utilized in the evaluation of cardiac ATTR amyloidosis [14]. On the other hand, 11C-labeled Pittsburgh compound B (11C-PiB; 2-[4′-methylaminophenyl]-6-hydroxybenzothiazole) positron emission tomography (PET) was developed to evaluate localized Aβ amyloid deposition in the brains of patients with Alzheimer’s disease. Recently, our group showed that 11C-PiB PET can also detect ATTRv and AL amyloid deposition [15,16].
Quantification of cardiac amyloid with [18F]Flutemetamol in patients with V30M hereditary transthyretin amyloidosis
Published in Amyloid, 2020
Sofia Möckelind, Jan Axelsson, Björn Pilebro, Per Lindqvist, Ole B. Suhr, Torbjörn Sundström
For imaging of amyloid in patients with Alzheimer’s disease, a class of positron emission tomography (PET) tracers, originating from thioflavin T, have been developed. The original Carbon-11-labeled Pittsburgh compound B (11C-PIB) visualises amyloid deposition in the brain at an early stage of Alzheimer’s disease [20]. 11C-PIB and a fluorine-based tracer [18F]Florbetapir have in a few studies shown amyloid uptake outside of the brain [21] and both tracers have in different studies shown a high affinity for cardiac deposits in ATTR amyloidosis [22–24]. Pilebro et al. showed that ATTR fibril type B patients had a higher heart uptake of 11C-PIB [16] than those with fibril type A. [18F]Flutemetamol [25] has shown a similar uptake in the brain of patients with Alzheimer’s disease when compared to 11C-PIB [26]. A case study suggests [18F]Flutemetamol could be used in diagnostics of cardiac amyloidosis [27].