Adult Cognitive DiseaseThe research corpus Monographs

Cytoskeletal Collapse Node

Actin and microtubule cytoskeleton attacked by multiple mechanisms, leading to dendritic spine loss and synaptic failure.

Converging Mechanisms

  • LIMK1 hyperactivation and cofilin inactivation (Ramsden: GSK3beta cascade)
  • Ephexin5-RhoA-ROCK-mediated actin-myosin contraction (Margolis)
  • Competitive synaptic plasticity dysregulation (Huang)
  • Complement-mediated dendritic spine destruction (Shatz/Brott)

Key Molecules

GSK3beta, LIMK1, cofilin, Ephexin5, RhoA, ROCK, PSD95

To be populated after CSC grading.

See Also

Papers converging on this axis

8
Carlo Abbate's Adult Neurogenesis Theory of Alzheimer's Disease, Critically Evaluated 6 concepts · 1 gene shared Alzheimer's Disease as a Failure of Proteolytic Timing, Read Out at Cofilin Serine 3 5 concepts · 3 genes shared From Synapse Loss to Neuronal Death in Alzheimer's Disease 5 concepts · 3 genes shared Bess Frost's Chromatin Programme, the Elements It Releases, and the Restraint on cGAS 6 concepts shared cGAS–STING in Alzheimer's Disease 6 concepts shared Cortical Immature Neurons of Layer II 6 concepts shared Different Tau Strains Cause Different Diseases 6 concepts shared Solomon Carter Fuller's 1911 Plaque Audit, Read Beside Oskar Fischer's 6 concepts shared

Concepts on this axis

374
Abeta aggregation as necessary initiating eventAbeta as molecular prime moverAcyloxyacyl Hydrolase NeuroprotectionAD as a double prion disorderAD as accelerated aging of Abeta managementAD as accelerated normal agingAD as accumulation of insults exceeding homeostasisAD as clinical syndrome not diseaseAD as systemic disease not limited to brainAD caused by APP dysregulation not Abeta per seAdult hippocampal neurogenesis restorationAdult NeurogenesisAge-dependent feedback loops in neurodegenerationAge-dependent threshold modelAge-related immune dysfunction enables neurotropic virusesAging accelerators and deceleratorsAging as MechanismAging as root cause of ADAging-epigenetic-genetic interactionAI Disease Model DiscoveryAI Neurotherapeutic DiscoveryAI-based early diagnosisAluminum as primary environmental causeAluminum driving amyloid productionAmyloid and tau as secondary byproductsAmyloid and tau as secondary phenomenaAmyloid as age-related phenomenonAmyloid as antimicrobial defenseAmyloid as downstream secondaryAmyloid as secondary to synaptic dysfunctionAmyloid clearance as important as depositionAmyloid Clinical DisconnectAmyloid plaques as fibrotic scar tissue from BBB repairAmyloid structural diversity and toxicityAmyloid-beta as innate immune defenseAnti Ferroptotic BotanicalsAnti-prion therapeutics as novel drug strategyAntibody Target SpecificityAntimicrobial hypothesis of amyloidApoE isoform-heparin binding differences

Last reviewed 5 April 2026.

Important noticeThis is a research platform, not a medical site. Nothing here is medical advice, a diagnosis, or a treatment recommendation, and none of it has been reviewed by a regulator. The drugs, doses and trials discussed are research literature, not prescriptions. If dementia affects you or someone you care about, speak to a doctor.

Compiled from the knowledge base and the research corpus under the Organic Network Synthesis methodology · the research corpus of Adult Cognitive Disease · the seven monographs are here. 2026.

854 interlinked articles · 148 papers in full · 53 as typeset PDFs · 635 concepts · 7 convergence nodes · 5 temporal stages.

Discussion

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