ReviewBiological psychiatry2014
Alzheimer's disease: new data highlight nonneuronal cell types and the necessity for presymptomatic prevention strategies.
Review in Biological psychiatry, 2014. 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, 11 citations in OpenAlex.
- Alpha lipoic acid reverses scopolamine-induced spatial memory loss and pyramidal cell neurodegeneration in the prefrontal cortex of Wistar rats.IBRO neuroscience reports · 2022Article
- Associations Between Positron Emission Tomography Amyloid Pathology and Diffusion Tensor Imaging Brain Connectivity in Pre-Clinical Alzheimer's Disease.Brain connectivity · 2019Article
- Reactive Astrocytes as Drug Target in Alzheimer's Disease.BioMed research international · 2018Review
- Cerebrospinal fluid biomarkers of neurovascular dysfunction in mild dementia and Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Review
- Amyloid-beta protein clearance and degradation (ABCD) pathways and their role in Alzheimer's disease.Current Alzheimer research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Despite compelling genetic evidence indicating that cerebral amyloidosis can be, at least sometimes, the primary cause of Alzheimer's disease (AD), clinical trials for symptomatic AD with amyloid-reducing agents have succeeded at target engagement but failed to cause clinical benefit. In a landmark shift, the U.S. Food and Drug Administration now proposes to approve prophylaxis that alters the trajectory of what is now believed to be typical AD biomarker evolution. The first prevention trials are now beginning in patients with genetic guarantees for or high genetic risks for AD. The expectation is that clues to their outcomes will begin to emerge from these trials in approximately 2018. In the meantime, new strategies point to nonneuronal cells and to system pathology. A review of the current state of the art of AD science follows herein.
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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.