ReviewMolecular neurobiology2013
The senescence hypothesis of disease progression in Alzheimer disease: an integrated matrix of disease pathways for FAD and SAD.
Review in Molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Recent advances in potential enzymes and their therapeutic inhibitors for the treatment of Alzheimer's disease.Heliyon · 2024Review
- Prominent and conspicuous astrocyte atrophy in human sporadic and familial Alzheimer's disease.Brain structure & function · 2023Article
- Review
- Chinese herbal compound Jinsiwei improves synaptic plasticity in mice with sporadic Alzheimer's disease induced by streptozotocin.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
- Induction of Brain Insulin Resistance and Alzheimer's Molecular Changes by Western Diet.International journal of molecular sciences · 2022Article
- Amyloid in the ageing brain: New frameworks and perspectives.Aging brain · 2021Article
- Cellular senescence and Alzheimer disease: the egg and the chicken scenario.Nature reviews. Neuroscience · 2020Review
- The puzzle of preserved cognition in the oldest old.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020Review
- Interleukin-1β Drives Cellular Senescence of Rat Astrocytes Induced by Oligomerized Amyloid β Peptide and Oxidative Stress.Frontiers in neurology · 2020Article
- A post-translational modification signature defines changes in soluble tau correlating with oligomerization in early stage Alzheimer's disease brain.Acta neuropathologica communications · 2019Article
- Understanding the roles of mutations in the amyloid precursor protein in Alzheimer disease.Molecular psychiatry · 2018Review
- Involvement of insulin resistance in D-galactose-induced age-related dementia in rats: Protective role of metformin and saxagliptin.PloS one · 2017Article
- Dissecting the Contribution of Vascular Alterations and Aging to Alzheimer's Disease.Molecular neurobiology · 2016Review
- Alzheimer's Disease: Mechanism and Approach to Cell Therapy.International journal of molecular sciences · 2015Review
- The case for rejecting the amyloid cascade hypothesis.Nature neuroscience · 2015Review
- Iron chelation and multiple sclerosis.ASN neuro · 2014Review
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer disease (AD) is a progressive, neurodegenerative disease characterised in life by cognitive decline and behavioural symptoms and post-mortem by the neuropathological hallmarks including the microtubule-associated protein tau-reactive tangles and neuritic plaques and amyloid-beta-protein-reactive senile plaques. Greater than 95 % of AD cases are sporadic (SAD) with a late onset and <5 % of AD cases are familial (FAD) with an early onset. FAD is associated with various genetic mutations in the amyloid precursor protein (APP) and the presenilins (PS)1 and PS2. As yet, no disease pathway has been fully accepted and there are no treatments that prevent, stop or reverse the cognitive decline associated with AD. Here, we review and integrate available environmental and genetic evidence associated with all forms of AD. We present the senescence hypothesis of AD progression, suggesting that factors associated with AD can be seen as partial stressors within the matrix of signalling pathways that underlie cell survival and function. Senescence pathways are triggered when stressors exceed the cells ability to compensate for them. The APP proteolytic system has many interactions with pathways involved in programmed senescence and APP proteolysis can both respond to and be driven by senescence-associated signalling. Disease pathways associated with sporadic disease may be different to those involving familial genetic mutations. The interpretation we provide strongly points to senescence as an additional underlying causal process in dementia progression in both SAD and FAD via multiple disease pathways.
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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.