ReviewCold Spring Harbor perspectives in medicine2012
Physiological functions of APP family proteins.
Review in Cold Spring Harbor perspectives in medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 2 of them syntheses that pooled it.
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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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.
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Who cites it
165 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Genetic and environmental risk factors for dementia in African adults: A systematic review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Pooled it
- Network-based gene deletion analysis identifies candidate genes and molecular mechanism involved in clear cell renal cell carcinoma.Journal of genetics · 2021Pooled it
- Combinatorial mechanisms specify cellular location and neurotransmitter identity during planarian neurogenesis.Nature communications · 2026Article
- Pathological or preventative? Amyloid-β as an effector of innate immunity.Infection and immunity · 2026Review
- Protein networks are influenced by maternal BMI and differentiate preterm birth types.Communications medicine · 2026Article
- Magnetoreceptive CRY/MagR complexes: linking circadian redox signalling to protein aggregation in Alzheimer's and Parkinson's disease.ADMET & DMPK · 2026Review
- APP E590D mutation increases generation of Aβ and Aη peptides and exacerbates tauopathy.NPJ dementia · 2026Article
- Prenatal Exposure To Valproic Acid Induces Increased Autism-Like Behaviors and Impairment of Learning and Memory Functions in Rat Offspring by Upregulating ADAM10 Expression.Neurochemical research · 2025Article
- Inducers and modulators of protein aggregation in Alzheimer's disease - Critical tools for understanding the foundations of aggregate structures.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Astrocyte-to-neuron HNature metabolism · 2025Article
- Identification of hub genes in congenital hypothyroidism and construction of the associated immune regulatory network.Frontiers in immunology · 2025Article
- Article
- Protein modification in neurodegenerative diseases.MedComm · 2024Review
- Alpha-lipoic acid alleviates cognitive deficits in transgenic APP23/PS45 mice through a mitophagy-mediated increase in ADAM10 α-secretase cleavage of APP.Alzheimer's research & therapy · 2024Article
- Aplp1 interacts with Lag3 to facilitate transmission of pathologic α-synuclein.Nature communications · 2024Article
- Label-free detection of Aβ-42: a liquid crystal droplet approach for Alzheimer's disease diagnosis.RSC advances · 2024Article
- Skeletal muscle as a molecular and cellular biomarker of disease progression in amyotrophic lateral sclerosis: a narrative review.Neural regeneration research · 2024Review
- Exploring Heparan Sulfate Proteoglycans as Mediators of Human Mesenchymal Stem Cell Neurogenesis.Cellular and molecular neurobiology · 2024Review
- Differential patterns of lysosomal dysfunction are seen in the clinicopathological forms of primary progressive aphasia.Journal of neurology · 2024Article
- Genetic and chemical disruption of amyloid precursor protein processing impairs zebrafish sleep maintenance.iScience · 2024Article
105 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Biochemical and genetic evidence establishes a central role of the amyloid precursor protein (APP) in Alzheimer disease (AD) pathogenesis. Biochemically, deposition of the β-amyloid (Aβ) peptides produced from proteolytic processing of APP forms the defining pathological hallmark of AD; genetically, both point mutations and duplications of wild-type APP are linked to a subset of early onset of familial AD (FAD) and cerebral amyloid angiopathy. As such, the biological functions of APP and its processing products have been the subject of intense investigation, and the past 20+ years of research have met with both excitement and challenges. This article will review the current understanding of the physiological functions of APP in the context of APP family members.
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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.