ReviewInternational journal of molecular sciences2018
Presenilins as Drug Targets for Alzheimer's Disease-Recent Insights from Cell Biology and Electrophysiology as Novel Opportunities in Drug Development.
Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 23 citations in OpenAlex.
- Comprehending Alzheimer's Disease: Molecular Mechanisms and Treatment Strategies.Current Alzheimer research · 2025Review
- Untangling the Genetic Threads of Alzheimer's: Insights into Risk Factors and Biomarkers.Current gene therapy · 2025Review
- Gamma secretase activity modulates BMP-7-induced dendritic growth in primary rat sympathetic neurons.Autonomic neuroscience : basic & clinical · 2023Article
- Guizhi Fuling capsule relieves memory deficits by inhibition of microglial neuroinflammation through blocking JAK2/STAT3 pathway in presenilin1/2 conditional double knockout mice.Frontiers in immunology · 2023Article
- Genetics, Functions, and Clinical Impact of Presenilin-1 (PSEN1) Gene.International journal of molecular sciences · 2022Review
- The interplay between oxidative stress and autophagy: focus on the development of neurological diseases.Behavioral and brain functions : BBF · 2022Review
- Nanomedicines in the Management of Alzheimer's Disease: Current View and Future Prospects.Frontiers in aging neuroscience · 2022Review
- Diagnostic Utility of Selected Serum Dementia Biomarkers: Amyloid β-40, Amyloid β-42, Tau Protein, and YKL-40: A Review.Journal of clinical medicine · 2020Review
- A Comprehensive Review of Alzheimer's Association with Related Proteins: Pathological Role and Therapeutic Significance.Current neuropharmacology · 2020Review
- The Interplay between CaInternational journal of molecular sciences · 2019Review
- NGP 555, a γ-secretase modulator, shows a beneficial shift in the ratio of amyloid biomarkers in human cerebrospinal fluid at safe doses.Alzheimer's & dementia (New York, N. Y.) · 2019Article
- Non-coding RNA influences in dementia.Non-coding RNA research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A major cause underlying familial Alzheimer's disease (AD) are mutations in presenilin proteins, presenilin 1 (PS1) and presenilin 2 (PS2). Presenilins are components of the γ-secretase complex which, when mutated, can affect amyloid precursor protein (APP) processing to toxic forms of amyloid beta (Aβ). Consequently, presenilins have been the target of numerous and varied research efforts to develop therapeutic strategies for AD. The presenilin 1 gene harbors the largest number of AD-causing mutations resulting in the late onset familial form of AD. As a result, the majority of efforts for drug development focused on PS1 and Aβ. Soon after the discovery of the major involvement of PS1 and PS2 in γ-secretase activity, it became clear that neuronal signaling, particularly calcium ion (Ca
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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.