ReviewDer Nervenarzt2019
[Did Alzheimer research fail entirely? : Failure of amyloid-based clinical studies].
Review in Der Nervenarzt, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- [Disease-modifying treatment approaches for Alzheimer's disease].Der Nervenarzt · 2021Review
- The Rhesus Macaque as a Translational Model for Neurodegeneration and Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Amyloidosis increase is not attenuated by long-term calorie restriction or related to neuron density in the prefrontal cortex of extremely aged rhesus macaques.GeroScience · 2020Article
- [Gene-specific treatment approaches in Alzheimer's disease and other tauopathies].Der Nervenarzt · 2020Review
- Is γ-secretase a beneficial inactivating enzyme of the toxic APP C-terminal fragment C99?The Journal of biological chemistryReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Numerous amyloid-based clinical studies have recently failed. Does this mean that the mechanisms of Alzheimer's disease have to be reinvestigated and that amyloid is not the trigger of the disease? Strong genetic evidence from familial Alzheimer's disease contradicts this fatalistic opinion. Mutations in all genes associated with familial Alzheimer's disease affect amyloid metabolism and aggregation. Moreover, a protective mutation reduces amyloid production by 20-30% throughout the lifetime. Clinical studies rather failed because secretase inhibitors block cleavage of numerous other physiologically important substrates of secretases. Moreover, the disease is initiated decades before symptoms occur. Successful treatment attempts with anti-amyloid medication based on other prototype amyloidoses are described. Finally, new therapeutic target molecules expressed in microglia cells are discussed.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.