The bivariate distribution of amyloid- β and tau: relationship with established neurocognitive clinical syndromes

We examined these clinical groups in relation to the bivariate distribution of amyloid and tau PET values. Individuals were grouped into amyloid (A)/tau (T) quadrants based on previously established abnormality cut points of s tandardized uptake value ratio 1.48 (A) and 1.33 (T). Individual participants largely fell into one of three amyloid/tau quadrants: low amyloid and low tau (A−T−), high amyloid and low tau (A+T−), or high amyloid and high tau (A+T+). Seventy per cent of cognitively unimpaired and 74% of FTD pa rticipants fell into the A−T− quadrant. Participants with mild cognitive impairment spanned the A−T− (42%), A+T− (28%), and A+T+ (27%) quadrants. Probable dementia with Lewy body participants spanned the A−T− (38%) and A+T− (44%) quadrants. Most (89%) participants with Alzheimer clin ical syndrome fell into the A+T+ quadrant. These data support several conclusions. First, among 1343 participants, abnormal tau PET rarely occurred in the absence of abnormal amyloid PET, but the reverse was common. Thus, with rare exceptions, amyloidosis appears to be required for high levels of 3R /4R tau deposition. Second, abnormal amyloid PET is compatible with normal cognition but highly abnormal tau PET is not. These two conclusions support a dynamic biomarker model in which Alzheimer’s disease is characterized first by the appearance of amyloidosis and later by tauopathy, with tauopat hy being the proteino...
Source: Brain - Category: Neurology Source Type: research

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Intra-gastrointestinal amyloid-β1-42 oligomers perturb enteric function and induce Alzheimer's disease pathology. J Physiol. 2020 Jul 02;: Authors: Sun Y, Sommerville NR, Liu JYH, Ngan MP, Poon D, Ponomarev ED, Lu Z, Kung JSC, Rudd JA Abstract KEY POINTS: Alzheimer's disease (AD) patients and transgenic mice have beta-amyloid (Aβ) aggregation in the gastrointestinal (GI) tract. It is possible that Aβ from the periphery contributes to the load of Aβ in the brain, as Aβ has prion-like properties. The present investigations demonstrate that Aβ injected into the GI tract of I...
Source: The Journal of Physiology - Category: Physiology Authors: Tags: J Physiol Source Type: research
Pathogenic tau triggers tauopathy, which serves as a focal point for many other neurodegenerative diseases. Nanogold polyethylene glycol(Au ‐PEG) alters tau as a nanochaperon and lowers protopathic tau burden while also acting as kinetic stabilizer preventing tau oligomerization. Au‐PEG inhibits amyloidosis in human AD serum by remodeling tau‐like pro‐dementia factors. Editing tau function by Au‐PEG brings optimism to managing Alzheimer's dementia. AbstractTauopathy is a complex disorder associated at the junction of several other pathologies. Intrinsically disordered tau protein remains therapeutically challengi...
Source: Small - Category: Nanotechnology Authors: Tags: Communication Source Type: research
We report a new class of natural-product-inspired covalent inhibitors of telomerase that target the catalytic active site. Age-Related Epigenetic Changes that Suppress Mitochondrial Function https://www.fightaging.org/archives/2020/03/age-related-epigenetic-changes-that-suppress-mitochondrial-function/ Today's open access research reports on two specific epigenetic changes observed in old individuals that act to reduce mitochondrial function. This joins an existing list of genes for which expression changes are known to impact mitochondrial function with age. A herd of hundreds of mitochondria are found ...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
Alzheimer's disease is characterized by the presence of protein aggregates in the brain. These are misfolded and altered versions of proteins that can act as seeds for solid deposits to form and spread in the brain. These deposits are surrounded by a halo of toxic biochemistry that harms and eventually kills neurons. Amyloid-β aggregates are present in the early stages of the condition, while tau aggregates cause much greater harm and cell death in the later stages. Alzheimer's disease is also an inflammatory condition, however, in which chronic inflammation and altered behavior of the central nervous system im...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs
In Reply The Letter to the Editor by Montero-Odasso and colleagues addresses noncognitive manifestations of Alzheimer disease (AD). Their letter discusses a recent article from the Mayo Clinic. Using positron emission tomography biomarkers of amyloidosis (A) and tauopathy (T), the Mayo study examined the age- and sex-specific prevalence of 3 biologically defined entities: amyloidosis (A+) regardless of tau status, A+T −, and A+T+. We compared the age and sex specific prevalence of these 3 biomarker-defined entities with 3 clinical syndromes commonly associated with AD: clinically defined probable AD using the McKhann...
Source: JAMA Neurology - Category: Neurology Source Type: research
In the progression of Alzheimer ’s disease (AD), subtle cognitive difficulties may develop prior to or alongside the early phases of amyloid accumulation, according to astudy published Monday inNeurology. The findings challenge the hypothesis that amyloidosis (the buildup of amyloid proteins) comes first in the Alzheimer ’s disease process.Kelsey R. Thomas, Ph.D., of the VA San Diego Healthcare System and colleagues analyzed data from 747 people aged 55 to 90 without dementia who participated in theAlzheimer ’s Disease Neuroimaging Initiative. The participants received PET imaging to determine amyloid lev...
Source: Psychiatr News - Category: Psychiatry Tags: Adam M. Brickman Alzheimer's disease amyloid attention Beth E. Snitz entorhinal cortex Kelsy Thomas language memory mild cognitive impairment Neurology Source Type: research
Fight Aging! publishes news and commentary relevant to the goal of ending all age-related disease, to be achieved by bringing the mechanisms of aging under the control of modern medicine. This weekly newsletter is sent to thousands of interested subscribers. To subscribe or unsubscribe from the newsletter, please visit: https://www.fightaging.org/newsletter/ Longevity Industry Consulting Services Reason, the founder of Fight Aging! and Repair Biotechnologies, offers strategic consulting services to investors, entrepreneurs, and others interested in the longevity industry and its complexities. To find out m...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
We examined, in a community-based population (N = 777, aged 50–95) (1) what variables were associated with each of the CSF (N) markers, and (2) whether the variables associated with each marker differed by increased brain amyloid. CSF T-tau was measured with an automated electrochemiluminescence Elecsys immunoassay; NfL and Ng were measured with in-house enzyme-linked immunosorbent assays.ResultsMultiple variables were differentially associated with CSF NfL and T-tau levels, but not Ng. Most associations were attenuated after adjustment for age and sex. T-tau had the strongest association with cognition in ...
Source: Alzheimer's and Dementia: The Journal of the Alzheimer's Association - Category: Geriatrics Source Type: research
In conclusion, in the absence of obesity, visceral adipose tissue possesses a pronounced anti-inflammatory phenotype during aging which is further enhanced by exercise. Methods of Inducing Cellular Damage are Rarely Relevant to Aging, and the Details Matter https://www.fightaging.org/archives/2019/08/methods-of-inducing-cellular-damage-are-rarely-relevant-to-aging-and-the-details-matter/ One of the major challenges in aging research is determining whether or not models of cellular or organismal damage and its consequences are in any way relevant to the natural processes of aging. One can hit a brick with...
Source: Fight Aging! - Category: Research Authors: Tags: Newsletters Source Type: blogs
CONCLUSIONS: We highlight the frequent presence of amyloid pathology in prodromal LBD in our population, and the probable involvement of different metabolic pathways in the same clinically defined dementia. PMID: 31309997 [PubMed - in process]
Source: Revista de Neurologia - Category: Neurology Authors: Tags: Rev Neurol Source Type: research
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