ReviewMetabolic brain disease2025
Resilience mechanisms underlying Alzheimer's disease.
Review in Metabolic brain disease, 2025. 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
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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.
- Alzheimer's Disease Neuropathological characterization of the dog brain and relationship to biofluid biomarkers and cognitive function.Research square · 2026Article
- Alzheimer's disease neuropathological characterization of the dog brain and relationship to biofluid biomarkers and cognitive function.NPJ dementia · 2026Article
- The Endocannabinoid-Microbiota-Neuroimmune Super-System: A Unifying Feedback Architecture for Systems Resilience, Collapse Trajectories, and Precision Feedback Medicine.International journal of molecular sciences · 2025Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) consists of two main pathologies, which are the deposition of amyloid plaque as well as tau protein aggregation. Evidence suggests that not everyone who carries the AD-causing genes displays AD-related symptoms; they might never acquire AD as well. These individuals are referred to as non-demented individuals with AD neuropathology (NDAN). Despite the presence of extensive AD pathology in their brain, it was found that NDAN had better cognitive function than was expected, suggesting that they were more resilient (better at coping) to AD due to differences in their brains compared to other demented or cognitively impaired patients. Thus, identification of the mechanisms underlying resilience is crucial since it represents a promising therapeutic strategy for AD. In this review, we will explore the molecular mechanisms underpinning the role of genetic and molecular resilience factors in improving resilience to AD. These include protective genes and proteins such as APOE2, BDNF, RAB10, actin network proteins, scaffolding proteins, and the basal forebrain cholinergic system. A thorough understanding of these resilience mechanisms is crucial for not just comprehending the development of AD but may also open new treatment possibilities for AD by enhancing the neuroprotective pathway and targeting the pathogenic process.
Indexed as
Identifiers
39760900What Socratic 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 Socratic graph.