Amyloid-β and Tau

Bloom, George S.

doi:10.1001/jamaneurol.2013.5847

Cited by 1,530 publications

(706 citation statements)

References 43 publications

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“…Although it is still under debate if neurodegeneration underlies tau‐dependent A β toxicity or A β ‐dependent tau toxicity,13 there is convincing evidence that the amount and distribution of tau correlates with the severity and the duration of dementia,14 underscoring the independent contribution of tau pathology.…”

Section: Discussionmentioning

confidence: 99%

Impact of tau and amyloid burden on glucose metabolism in Alzheimer's disease

Bischof

Jessen

Fließbach

et al. 2016

Ann Clin Transl Neurol

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In a multimodal PET imaging approach, we determined the differential contribution of neurofibrillary tangles (measured with [18F]AV‐1451) and beta‐amyloid burden (measured with [11C]PiB) on degree of neurodegeneration (i.e., glucose metabolism measured with [18F]FDG‐PET) in patients with Alzheimer's disease. Across brain regions, we observed an interactive effect of beta‐amyloid burden and tau deposition on glucose metabolism which was most pronounced in the parietal lobe. Elevated beta‐amyloid burden was associated with a stronger influence of tau accumulation on glucose metabolism. Our data provide the first in vivo insights into the differential contribution of Aβ and tau to neurodegeneration in Alzheimer's disease.

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Section: Discussionmentioning

confidence: 99%

Impact of tau and amyloid burden on glucose metabolism in Alzheimer's disease

Bischof

Jessen

Fließbach

et al. 2016

Ann Clin Transl Neurol

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“…The failure of these studies has caused some to consider that concurrent treatment for multiple protein abnormalities may be necessary in AD, where the importance of both amyloid and tau are well established (Bloom, 2014). The current findings extend this logic to FTLD and suggest that treatment for both amyloid and whatever FTLD protein is involved in each patient may be necessary to treat all factors leading to neurodegeneration.…”

Section: Discussionmentioning

confidence: 72%

O4‐01‐04: Amyloid in Dementia Associated With Familial Ftld: Not an Innocent Bystander

Naasan

Rosen

Rabinovici

et al. 2014

Alzheimer's & Dementia

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Patients with frontotemporal lobar degeneration (FTLD) can show superimposed amyloid pathology, though the impact of amyloid on the clinical presentation of FTLD is not well characterized. This cross-sectional case-control study compared clinical features, fluorodeoxyglucose-positron emission tomography metabolism and gray matter volume loss in 30 patients with familial FTLD in whom amyloid status was confirmed with autopsy or Pittsburgh compound B-PET. Compared to the amyloid-negative patients, the amyloid-positive patients performed significantly worse on several cognitive tests and showed hypometabolism and volume loss in more temporoparietal regions. Our results suggest that in FTLD amyloid positivity is associated with a more Alzheimer's disease-like pattern of neurodegeneration.

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“…Aside from extracellular amyloid plaques, also intraneuronal neurofibrillary tangles mainly comprised of the microtubule‐associated protein tau, are a morphological feature of AD brains 200, 201, 202. There is evidence that A β partly executes its cytotoxicity upstream of tau hyperphosphorylation and subsequent self‐assembly 203, 204.…”

Section: Degenerative Pathomechanisms In Ibmmentioning

confidence: 99%

Immune and myodegenerative pathomechanisms in inclusion body myositis

Keller

Schmidt

Lünemann

2017

Ann Clin Transl Neurol

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Inclusion Body Myositis (IBM) is a relatively common acquired inflammatory myopathy in patients above 50 years of age. Pathological hallmarks of IBM are intramyofiber protein inclusions and endomysial inflammation, indicating that both myodegenerative and inflammatory mechanisms contribute to its pathogenesis. Impaired protein degradation by the autophagic machinery, which regulates innate and adaptive immune responses, in skeletal muscle fibers has recently been identified as a potential key pathomechanism in IBM. Immunotherapies, which are successfully used for treating other inflammatory myopathies lack efficacy in IBM and so far no effective treatment is available. Thus, a better understanding of the mechanistic pathways underlying progressive muscle weakness and atrophy in IBM is crucial in identifying novel promising targets for therapeutic intervention. Here, we discuss recent insights into the pathomechanistic network of mutually dependent inflammatory and degenerative events during IBM.

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Amyloid-β and Tau

Cited by 1,530 publications

References 43 publications

Impact of tau and amyloid burden on glucose metabolism in Alzheimer's disease

Impact of tau and amyloid burden on glucose metabolism in Alzheimer's disease

O4‐01‐04: Amyloid in Dementia Associated With Familial Ftld: Not an Innocent Bystander

Immune and myodegenerative pathomechanisms in inclusion body myositis

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