ReviewTranslational research : the journal of laboratory and clinical medicine2014
Regenerative medicine in Alzheimer's disease.
Review in Translational research : the journal of laboratory and clinical medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 43 citations in OpenAlex.
- Article
- Stem Cells in Regenerative Medicine: A Journey from Adult Stem Cells to Induced Pluripotent Cells.International journal of molecular sciences · 2025Review
- Review
- Article
- Exploring the efficacy of natural products in alleviating Alzheimer's disease.Neural regeneration research · 2019Review
- Minimally Invasive and Regenerative Therapeutics.Advanced materials (Deerfield Beach, Fla.) · 2019Review
- A novel strategy to achieve effective drug delivery: exploit cells as carrier combined with nanoparticles.Drug delivery · 2017Review
- Perspective: Neuroregenerative Nutrition.Advances in nutrition (Bethesda, Md.) · 2017Article
- Polysaccharides from Ganoderma lucidum Promote Cognitive Function and Neural Progenitor Proliferation in Mouse Model of Alzheimer's Disease.Stem cell reports · 2017Article
- Commentary: L-3-n-butylphthalide Rescues Hippocampal Synaptic Failure and Attenuates Neuropathology in Aged APP/PS1 Mouse Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2017Article
- L-3-n-butylphthalide Rescues Hippocampal Synaptic Failure and Attenuates Neuropathology in Aged APP/PS1 Mouse Model of Alzheimer's Disease.CNS neuroscience & therapeutics · 2016Article
- Recent Advances in Neurogenic Small Molecules as Innovative Treatments for Neurodegenerative Diseases.Molecules (Basel, Switzerland) · 2016Review
- Associations between Sleep, Cortisol Regulation, and Diet: Possible Implications for the Risk of Alzheimer Disease.Advances in nutrition (Bethesda, Md.) · 2016Review
- New approaches to treating Alzheimer's disease.Perspectives in medicinal chemistry · 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Identifying novel, effective therapeutics for Alzheimer's disease (AD) is one of the major unmet medical needs for the coming decade. Because the current paradigm for developing and testing disease-modifying AD therapies is protracted and likely to be even longer, with the shift toward earlier intervention in preclinical AD, it is an open issue whether we can develop, test, and widely deploy a novel therapy in time to help the current at-risk generation if we continue to follow the standard paradigms of discovery and drug development. There is an imperative need to find safe and effective preventive measures that can be distributed rapidly to stem the coming wave of AD that will potentially engulf the next generation. We can define regenerative medicine broadly as approaches that use stem cell-based therapies or approaches that seek to modulate inherent neurogenesis. Neurogenesis, although most active during prenatal development, has been shown to continue in several small parts of the brain, including the hippocampus and the subventricular zone, suggesting its potential to reverse cognitive deficits. If AD pathology affects neurogenesis, then it follows that conditions that stimulate endogenous neurogenesis (eg, environmental stimuli, physical activity, trophic factors, cytokines, and drugs) may help to promote the regenerative and recovery process. Herein, we review the complex logistics of potentially implementing neurogenesis-based therapeutic strategies for the treatment of AD.
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.