ReviewFrontiers in molecular neuroscience2017
Alzheimer's Disease: From Genetic Variants to the Distinct Pathological Mechanisms.
Review in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed.
- Multi-dimensional attention framework for personalised Alzheimer's disease progression prediction across sporadic and genetic risk cohorts.Research square · 2026Article
- Modeling Alzheimer's Disease: A Review of Gene-Modified and Induced Animal Models, Complex Cell Culture Models, and Computational Modeling.Brain sciences · 2025Review
- Exosomal MicroRNAs in Alzheimer's Disease: Unveiling Their Role and Pioneering Tools for Diagnosis and Treatment.Journal of clinical medicine · 2024Review
- Review
- Vagus nerve stimulation in dementia: A scoping review of clinical and pre-clinical studies.AIMS neuroscience · 2024Article
- Mitochondrial Quality Control via Mitochondrial Unfolded Protein Response (mtUPR) in Ageing and Neurodegenerative Diseases.Biomolecules · 2023Review
- Recent Mechanisms of Neurodegeneration and Photobiomodulation in the Context of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Research progress on vestibular dysfunction and visual-spatial cognition in patients with Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- Gut metabolite trimethylamineFrontiers in aging neuroscience · 2022Article
- Triggering Innate Immune Receptors as New Therapies in Alzheimer's Disease and Multiple Sclerosis.Cells · 2021Review
- Mutations in the COPI coatomer subunit α-COP induce release of Aβ-42 and amyloid precursor protein intracellular domain and increase tau oligomerization and release.Neurobiology of aging · 2021Article
- Ferulic Acid Ameliorates Alzheimer's Disease-like Pathology and Repairs Cognitive Decline by Preventing Capillary Hypofunction in APP/PS1 Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Change in the plasma proteome associated with canine cognitive dysfunction syndrome (CCDS) in Thailand.BMC veterinary research · 2021Article
- Neurodegenerative Proteinopathies in the Proteoform Spectrum-Tools and Challenges.International journal of molecular sciences · 2021Review
- Does the CD33 rs3865444 Polymorphism Confer Susceptibility to Alzheimer's Disease?Journal of molecular neuroscience : MN · 2020Article
- The firstGigaByte (Hong Kong, China) · 2020Article
- Association of Genes Involved in the Metabolic Pathways of Amyloid-β and Tau Proteins With Sporadic Late-Onset Alzheimer's Disease in the Southern Han Chinese Population.Frontiers in aging neuroscience · 2020Article
- On the Conformational Dynamics of β-Amyloid Forming Peptides: A Computational Perspective.Frontiers in bioengineering and biotechnology · 2020Review
- Alterations in Alzheimer's Disease-Associated Gene Expression in Severe Obstructive Sleep Apnea Patients.Journal of clinical medicine · 2019Article
- Clinical features and genetic characteristics of two Chinese pedigrees with fatal family insomnia.Prion · 2019Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Being the most common cause of dementia, AD is a polygenic and neurodegenerative disease. Complex and multiple factors have been shown to be involved in its pathogenesis, of which the genetics play an indispensable role. It is widely accepted that discovery of potential genes related to the pathogenesis of AD would be of great help for the understanding of neurodegeneration and thus further promote molecular diagnosis in clinic settings. Generally, AD could be clarified into two types according to the onset age, the early-onset AD (EOAD) and the late-onset AD (LOAD). Progresses made by genetic studies on both EOAD and LOAD are believed to be essential not only for the revolution of conventional ideas but also for the revelation of new pathological mechanisms underlying AD pathogenesis. Currently, albeit the genetics of LOAD is much less well-understood compared to EOAD due to its complicated and multifactorial essence, Genome-wide association studies (GWASs) and next generation sequencing (NGS) approaches have identified dozens of novel genes that may provide insight mechanism of LOAD. In this review, we analyze functions of the genes and summarize the distinct pathological mechanisms of how these genes would be involved in the pathogenesis of AD.
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