ReviewCells2020
Presenilin-2 and Calcium Handling: Molecules, Organelles, Cells and Brain Networks.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 29 citations in OpenAlex.
- The emerging role of astrocytes in spatial cognition, action and Alzheimer's disease.Frontiers in cellular neuroscience · 2026Review
- Synaptic mitochondrial dysfunction and Alzheimer's disease: from molecular mechanisms to therapeutic strategies.Frontiers in pharmacology · 2026Review
- Presenilins as hub proteins controlling the endocytic and autophagic pathways and small extracellular vesicle secretion.Journal of extracellular vesicles · 2025Article
- The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- A Novel Rare PSEN2 Val226Ala in PSEN2 in a Korean Patient with Atypical Alzheimer's Disease, and the Importance of PSEN2 5th Transmembrane Domain (TM5) in AD Pathogenesis.International journal of molecular sciences · 2024Article
- Genetic Phenotypes of Alzheimer's Disease: Mechanisms and Potential Therapy.Phenomics (Cham, Switzerland) · 2023Review
- Review
- Rescue of astrocyte activity by the calcium sensor STIM1 restores long-term synaptic plasticity in female mice modelling Alzheimer's disease.Nature communications · 2023Article
- Article
- Cognitive- and memory-enhancing effects of Augmentin in Alzheimer's rats through regulation of gene expression and neuronal cell apoptosis.Frontiers in pharmacology · 2023Article
- Mitochondrial CaBiomedicines · 2022Review
- Excitotoxicity, calcium and mitochondria: a triad in synaptic neurodegeneration.Translational neurodegeneration · 2022Review
- Article
- Lighting Up CaCells · 2021Review
- Article
- Calcium Signalling in Alzheimer's Disease: From Pathophysiological Regulation to Therapeutic Approaches.Cells · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Presenilin-2 (PS2) is one of the three proteins that are dominantly mutated in familial Alzheimer's disease (FAD). It forms the catalytic core of the γ-secretase complex-a function shared with its homolog presenilin-1 (PS1)-the enzyme ultimately responsible of amyloid-β (Aβ) formation. Besides its enzymatic activity, PS2 is a multifunctional protein, being specifically involved, independently of γ-secretase activity, in the modulation of several cellular processes, such as Ca
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.