ReviewIranian journal of neurology2017
Taming Alzheimer's disease: New perspectives, newer horizons.
Review in Iranian journal of neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Co-nanoencapsulated meloxicam and curcumin improves cognitive impairment induced by amyloid-beta through modulation of cyclooxygenase-2 in mice.Neural regeneration research · 2021Article
- Sleep Disorders Associated With Alzheimer's Disease: A Perspective.Frontiers in neuroscience · 2018Review
- Analysis of Sleep Quality in People With Dementia: A Preliminary Study.Gerontology & geriatric medicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the leading cause of dementia. However, current therapies do not prevent progression of the disease. New research into the pathogenesis of the disease has brought about a greater understanding of the "amyloid cascade" and associated receptor abnormalities, the role of genetic factors, and revealed that the disease process commences 10 to 20 years prior to the appearance of clinical signs. This greater understanding of the disease has prompted development of novel disease-modifying therapies (DMTs) which may prevent onset or delay progression of the disease. Using genetic biomarkers like apolipoprotein E (ApoE) ε4, biochemical biomarkers like cerebrospinal fluid (CSF) amyloid and tau proteins, and imaging biomarkers like magnetic resonance imaging (MRI) and positron emission tomography (PET), it is now possible to detect preclinical AD and also monitor its progression in asymptomatic people. These biomarkers can be used in the selection of high-risk populations for clinical trials and also to monitor the efficacy and side-effects of DMT. To validate and standardize these biomarkers and select the most reliable, repeatable, easily available, cost-effective and complementary options is the challenge ahead.
Indexed as
Identifiers
29114370PMC5673987W2728658175What 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.