ReviewInternational journal of molecular sciences2009
Molecular pathogenesis of Alzheimer's disease: reductionist versus expansionist approaches.
Review in International journal of molecular sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 55 citations in OpenAlex.
- Quo Vadis translational neuroscience?Translational neuroscience · 2026Review
- Marine-derived Compounds: A Powerful Platform for the Treatment of Alzheimer's Disease.Central nervous system agents in medicinal chemistry · 2024Review
- Aluminium Induced Neurodegeneration in Rat Cerebellum in the Presence of Ethanol Coexposure.Journal of pharmacy & bioallied sciences · 2021Article
- Dementia screening of geriatric patients by implementing an informant-based Alzheimer's disease eight-item tool in KSA.Journal of Taibah University Medical Sciences · 2021Article
- Tocotrienol Rich Fraction Supplementation Modulate Brain Hippocampal Gene Expression in APPswe/PS1dE9 Alzheimer's Disease Mouse Model.Journal of Alzheimer's disease : JAD · 2019Article
- Excess cerebral TNF causing glutamate excitotoxicity rationalizes treatment of neurodegenerative diseases and neurogenic pain by anti-TNF agents.Journal of neuroinflammation · 2016Review
- APOε2 and education in cognitively normal older subjects with high levels of AD pathology at autopsy: findings from the Nun Study.Oncotarget · 2015Article
- Molecular Targets in Alzheimer's Disease: From Pathogenesis to Therapeutics.BioMed research international · 2015Review
- Our "energy-Ca(2+) signaling deficits" hypothesis and its explanatory potential for key features of Alzheimer's disease.Frontiers in aging neuroscience · 2014Article
- Neuropathological approaches to cerebral aging and neuroplasticity.Dialogues in clinical neuroscience · 2013Review
- Yizhijiannao Granule and a combination of its effective monomers, icariin and Panax notoginseng saponins, inhibit early PC12 cell apoptosis induced by beta-amyloid (25-35).Neural regeneration research · 2012Article
- Early post-natal iron administration induces astroglial response in the brain of adult and aged rats.Neurotoxicity research · 2011Article
- Screening of treatment targets for Alzheimer's disease from the molecular mechanisms of impairment by β-amyloid aggregation and tau hyperphosphorylation.Neuroscience bulletin · 2011Review
- Augmentation of aluminum-induced oxidative stress in rat cerebrum by presence of pro-oxidant (graded doses of ethanol) exposure.Neurochemical research · 2010Article
- Basic mechanisms of neurodegeneration: a critical update.Journal of cellular and molecular medicine · 2010Review
- Changes in the expression of genes associated with intraneuronal amyloid-beta and tau in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2010Article
- Does Alzheimer's disease begin in the brainstem?Neuropathology and applied neurobiology · 2009Article
- Recent advances in our understanding of neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2009Review
- Neurodegenerative disorders and nanoformulated drug development.Nanomedicine (London, England) · 2009Review
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 at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized clinically by dementia and pathologically by two hallmark lesions, senile plaques and neurofibrillary tangles. About a quarter century ago these hallmark lesions were purified and their protein constituents identified, precipitating an avalanche of molecular studies as well as substantial optimism about successful therapeutic intervention. In 2009, we now have copious knowledge on the biochemical cascades that produce these proteins, the different modifications and forms in which these proteins exist, and the ability to selectively target these proteins for therapeutic intervention on an experimental basis. At the same time, there has been no discernible alteration in the natural course of AD in humans. While it may be that the complexity of AD will exceed our capacity to make significant treatment progress for decades or more, a paradigm shift from the reductionism that defines amyloid-beta and tau hypotheses, to one that more accurately reflects the meaning of neuropathological changes, may be warranted. We and others have demonstrated that AD pathology is a manifestation of cellular adaptation, specifically as a defense against oxidative injury. As such, AD pathology is therefore a host response rather than a manifestation of cytotoxic protein injury, and is unlikely to be a fruitful target for therapeutic intervention. An "expansionist" view of the disease, we believe, with oxidative stress as a pleiotropic and upstream process, more aptly describes the relationship between various and numerous molecular alterations and clinical disease.
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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.