ArticleCurrent genomics2010
Functional genomics of brain aging and Alzheimer's disease: focus on selective neuronal vulnerability.
Article in Current genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Hippocampal transcriptome-wide association study and pathway analysis of mitochondrial solute carriers in Alzheimer's disease.Translational psychiatry · 2024Pooled it
- Neuronal HDAC9: A key regulator of cognitive and synaptic aging, rescuing Alzheimer's disease-related phenotypes.Molecular psychiatry · 2026Article
- Selective weakening of population-coupled synaptic activity in vivo in a mouse model of amyloid-beta pathology.Nature communications · 2026Article
- Recent Advancements in Neuroimaging-Based Alzheimer's Disease Prediction Using Deep Learning Approaches in e-Health: A Systematic Review.Health science reports · 2025Review
- Anti-inflammatory effects ofScientific reports · 2025Article
- Article
- Alzheimer's Disease: Exploring the Landscape of Cognitive Decline.ACS chemical neuroscience · 2024Review
- Deep learning techniques for Alzheimer's disease detection in 3D imaging: A systematic review.Health science reports · 2024Review
- Systematic Analysis of Biological Processes Reveals Gene Co-expression Modules Driving Pathway Dysregulation in Alzheimer's Disease.Aging and disease · 2024Article
- Systematic Analysis of Biological Processes Reveals Gene Co-expression Modules Driving Pathway Dysregulation in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
- Novel methodology for detection and prediction of mild cognitive impairment using resting-state EEG.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Adaptive responses of neuronal cells to chronic endoplasmic reticulum (ER) stress.Redox biology · 2023Article
- Cancer and Alzheimer's Inverse Correlation: an Immunogenetic Analysis.Molecular neurobiology · 2023Review
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- A protein-coding gene expression atlas from the brain of pregnant and non-pregnant goats.Frontiers in genetics · 2023Article
- Somatic copy number variant load in neurons of healthy controls and Alzheimer's disease patients.Acta neuropathologica communications · 2022Article
- The Brilliance of the Zebrafish Model: Perception on Behavior and Alzheimer's Disease.Frontiers in behavioral neuroscience · 2022Review
- The expression pattern of GDF15 in human brain changes during aging and in Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Preliminary exploration of the co-regulation of Alzheimer's disease pathogenic genes by microRNAs and transcription factors.Frontiers in aging neuroscience · 2022Article
- Cell competition from development to neurodegeneration.Disease models & mechanisms · 2021Review
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
Pivotal brain functions, such as neurotransmission, cognition, and memory, decline with advancing age and, especially, in neurodegenerative conditions associated with aging, such as Alzheimer's disease (AD). Yet, deterioration in structure and function of the nervous system during aging or in AD is not uniform throughout the brain. Selective neuronal vulnerability (SNV) is a general but sometimes overlooked characteristic of brain aging and AD. There is little known at the molecular level to account for the phenomenon of SNV. Functional genomic analyses, through unbiased whole genome expression studies, could lead to new insights into a complex process such as SNV. Genomic data generated using both human brain tissue and brains from animal models of aging and AD were analyzed in this review. Convergent trends that have emerged from these data sets were considered in identifying possible molecular and cellular pathways involved in SNV. It appears that during normal brain aging and in AD, neurons vulnerable to injury or cell death are characterized by significant decreases in the expression of genes related to mitochondrial metabolism and energy production. In AD, vulnerable neurons also exhibit down-regulation of genes related to synaptic neurotransmission and vesicular transport, cytoskeletal structure and function, and neurotrophic factor activity. A prominent category of genes that are up-regulated in AD are those related to inflammatory response and some components of calcium signaling. These genomic differences between sensitive and resistant neurons can now be used to explore the molecular underpinnings of previously suggested mechanisms of cell injury in aging and 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.