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Home › Research › Topics › plasticity

plasticity

287 studies tagged plasticity, dated 1983-02-20 to 2026-10-29. Bibliography: BibTeX (.bib) · RIS (.ris)

Newest in this topic

  1. Aβ42 oligomers disrupt calcium homeostasis via Piezo1 and induce neurotoxicity in differentiated SH-SY5Y cells 2026-10-29
  2. Endocannabinnoids innervate Circadian mechinary mitigating neuroinflammation, amyloidogenesis and cognition phenotypic to AD 2026-10-29
  3. Repeated VU0155069 Treatment Is Associated with Region- and Pathological Stage-Specific Dendritic Spine Remodeling in Female 3xTg-AD Mice 2026-10-27

Studies

287 studies carry this tag.

Date range

1983 to 2026

Top journals

  • The Journal of neuroscience : the official journal of the Society for Neuroscience 17
  • Nature neuroscience 10
  • Neuron 10
  • bioRxiv 10
  • Nature 8

137 journals in all.

Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.

  1. Aβ42 oligomers disrupt calcium homeostasis via Piezo1 and induce neurotoxicity in differentiated SH-SY5Y cells

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-29 Disease mechanisms

    Alzheimer's disease (AD) exhibits an intricate and multifactorial pathogenesis.

  2. Endocannabinnoids innervate Circadian mechinary mitigating neuroinflammation, amyloidogenesis and cognition phenotypic to AD

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Authorea Preprints 2026-10-29 Brain scans and imaging

    Constant LL exposure induced complete arrhythmicity and impaired recognition, working, and spatial reference memory.

  3. Repeated VU0155069 Treatment Is Associated with Region- and Pathological Stage-Specific Dendritic Spine Remodeling in Female 3xTg-AD Mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27 Brain tissue and pathology

    VU0155069 engages circuit- and pathological stage-specific forms of dendritic spine remodeling across distributed recognition- and associative-memory networks.

  4. Anti-GABA B receptor autoimmunity causes cognitive decline by presynaptic pathology

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-25 Disease mechanisms

    The GABA B receptor is a central regulator of neuronal transmission and excitability by pre- and postsynaptic mechanisms.

  5. Astrocytic ablation of truncated TrkB receptors reduces amyloid plaques and prevents synaptic loss in 5xFAD mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-24 Inflammation and the immune system

    Together, these findings identify astrocytic TrkB.T as an important regulator of amyloid pathology and synaptic integrity in an AD mouse model.

  6. GPR6 Protects Medial Entorhinal Cortex in 5×FAD Mice from Early Pathology in Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-22 Inflammation and the immune system

    Alzheimer’s disease (AD) is characterized by progressive memory decline, with the medial entorhinal cortex (MEC) representing an early vulnerable hub for spatial cognition.

  7. LATS2 modulates synaptic organization and function by regulating actin dynamics

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-19 Disease mechanisms

    Recent work has highlighted the importance of core Hippo pathway kinases in cycling cells.

  8. Reduced phosphatases and hyperphosphorylated glutamatergic receptors persist from early to late stages of prion disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-16 Disease mechanisms

    Synapse loss occurs early in prion disease, yet the intracellular signaling driving this dysregulation remains poorly understood.

  9. The protective effect of NGF mutant CHF6467 in SH SY5Y cells exposed to Aβ(1–42): a pharmacometabolomic approach

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-06 Vascular contributions

    Nerve Growth Factor (NGF) supports neuronal survival, plasticity, and growth by binding to p75NTR and TrkA receptors.

  10. PDE2A Modulation Attenuates Aβ-Induced Neuronal Injury and Associated Oxidative, Inflammatory, and Apoptotic Responses

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-01 Disease mechanisms

    Across cellular and animal Aβ injury models, BML-288 attenuated oxidative and inflammatory disturbances, modulated apoptosis-related protein expression, and improved cognitive outcomes.

  11. T1R2/T1R3 Identified as the Aβ Receptor: A New Mechanism Linking Aβ42/40 Ratio to Neuronal Hyperexcitability in Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-01 Biomarkers

    Early neuronal hyperexcitability is a hallmark of Alzheimer’s disease (AD) and correlates with cognitive decline.

  12. Endosomal pH Triggers Amyloid β Oligomerization and Maladaptive Phenotypic Plasticity in Alzheimers Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-28 Disease mechanisms

    Endosomal dysfunction is a presymptomatic hallmark of neurodegeneration.

  13. Aging and Alcohol Withdrawal Escalate CNS Hyperexcitability Across the Lifespan

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-24 Prevention and risk

    Central Nervous System (CNS) hyperexcitability is increased during aging and also during alcohol withdrawal.

  14. Postmortem Alterations of Metabotropic Glutamate Receptors across Neuropsychiatric Disorders: A Systematic Review

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-03 Prevention and risk

    Metabotropic glutamate receptors (mGluRs) regulate glutamatergic transmission and have been implicated in diverse neuropsychiatric disorders, but human postmortem evidence remains fragmented.

  15. The 25-Year Evolution of Lithium as a Disease-Modifying Agent in Dementia: A Narrative Review

    ✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA psychiatry 2026-09-01 Drug development

    These convergent data support a prospective clinical trial of low-dose lithium orotate to slow disease progression in MCI.

  16. Early Retinal UCHL1 Dysregulation Coupled With Synaptic Loss Reflects Alzheimer's Disease Severity

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2026-08-29 Disease mechanisms

    Synaptic dysfunction is a major driver of cognitive decline in Alzheimer's disease (AD), yet its extent and molecular basis in the retina remain poorly defined.

  17. Early Amyloid-β Toxicity Disrupts Nervous System Connectivity During Aging in Caenorhabditis elegans

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-29 Treatments

    Our experiments revealed that nAβ expressing animals exhibit a unique loss of positively correlated neuron connectivity, premature disruption of system wide dynamics, and reduced overall neuronal activity.

  18. Patient-Derived PSEN1 Cerebral Organoids Revealed Parallel Development of Amyloid-β Accumulation and Network Dysfunction

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Cellular and molecular neurobiology 2026-07-20 Biomarkers

    Alzheimer's disease (AD) is a neurodegenerative disorder characterised by progressive dementia, brain atrophy, and ultimately death.

  19. AETA peptide contributes to Alzheimer's disease signature of synapse dysfunction

    ✓ Peer-reviewed alzhub usefulness score 48 out of 100. Acta neuropathologica 2026-06-03 Disease mechanisms

    Alzheimer's disease (AD), the leading cause of dementia, is characterized by early synaptic dysfunction that precedes overt cognitive decline.

  20. Activation of neurogenesis improves amyloid-β pathology and cognitive function through AMP kinase signaling in Alzheimer’s disease model mice

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Cell reports 2025-12-26 Down syndrome and Alzheimer's

    Adult hippocampal neurogenesis declines with aging and in neurological disorders, leading to cognitive impairment.

  21. CSF biomarkers of neuroinflammation are associated with regional atrophy

    ✓ Peer-reviewed alzhub usefulness score 59 out of 100. Journal of neurology 2025-12-24 Inflammation and the immune system

    Higher synaptic latent factor (β = - 0.019, pFDR = 0.021) and YKL-40 (β = - 0.020, pFDR = 0.025) significantly predicted hippocampal atrophy.

  22. Direct evidence for dendritic spine compensation and regeneration in Alzheimer's disease models

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2025-10 Disease mechanisms

    We discovered that dendritic spine elimination-induced either artificially or in Aβ models-triggers a two-stage compensatory response: rapid enlargement of remaining spines followed by delayed spine regeneration.

  23. IRF1 ameliorates synaptic dysfunction through the modulation of O-GlcNAcylation on GluN1 subunit of NMDAR

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer's research & therapy 2025-09-30 Disease mechanisms

    In the present study, we demonstrate that Interferon Regulatory Factor-1 (IRF-1), which is deficient in the brain of individuals with Alzheimer's disease (AD), negatively regulates the O-GlcNAcylation levels of GluN1 through transcriptional regulation of the human OGA gene.

  24. Impaired Synaptic Plasticity Mechanisms in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Metabolic brain disease 2025-09-29 Disease mechanisms

    Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive cognitive decline driven by a complex interplay of genetic, environmental, and lifestyle factors.

  25. RNF168 dephosphorylation ameliorates cognitive decline in Aβ-based mouse models of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica communications 2025-09-24 Disease mechanisms

    Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder among the elderly, with limited effective treatments available in clinical practice.

  26. Adiponectin Receptor Agonist Ameliorates Synaptic Dysfunction in 3xTg Alzheimer's Disease Mouse Model by Activation of AMPK

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. CNS neuroscience & therapeutics 2025-09 Disease mechanisms

    Incubation of hippocampal slices with AdipoRon ameliorated long-term potentiation (LTP) and basal synaptic transmission deficits in 3xTg-AD mice.

  27. Impaired BDNF-TrkB trafficking and signalling in Down syndrome basal forebrain neurons

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Cell death & disease 2025-07-18 Down syndrome and Alzheimer's

    Brain derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) play crucial roles in neuronal development, synaptic transmission, and neuroplasticity.

  28. KChIP3 fosters neuroinflammation and synaptic dysfunction in the 5XFAD mouse model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of neuroinflammation 2025-06-19 Inflammation and the immune system

    Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by β-amyloid (βA) accumulation, neuroinflammation, excessive synaptic pruning, and cognitive decline.

  29. SFRP1 upregulation causes hippocampal synaptic dysfunction and memory impairment

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Cell reports 2025-04-07 Disease mechanisms

    Impaired neuronal and synaptic function are hallmarks of early Alzheimer's disease (AD), preceding other neuropathological traits and cognitive decline.

  30. Aerobic exercise improves clearance of amyloid-β via the glymphatic system in a mouse model of Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain research bulletin 2025-02-17 Prevention trials

    The funding showed that APP/PS1 mice have learning and memory impairment, and the glymphatic system is dysfunction.

  31. L-Lactate Administration Improved Synaptic Plasticity and Cognition in Early 3xTg-AD Mice

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. International journal of molecular sciences 2025-02-11 Disease mechanisms

    Synaptic plasticity impairment and behavioral deficits constitute classical pathological hallmarks in early-stage Alzheimer's disease (AD).

  32. Amyloid-β can activate JNK signalling via WNT5A-ROR2 to reduce synapse formation in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of cell science 2025-02-05 Biomarkers

    Wnt signalling is an essential signalling system in neurogenesis, with a crucial role in synaptic plasticity and neuronal survival, processes that are disrupted in Alzheimer's disease (AD).

  33. Targeted demethylation of cathepsin D via epigenome editing rescues pathology in Alzheimer's disease mouse model

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Theranostics 2025-01-01 Biomarkers

    Treatment with Ctsd-targeted dCas9-Tet1 in primary neurons overexpressing mutant APP (mutAPP) reduced Aβ peptide levels and the Aβ42/40 ratio.

  34. Long-term potentiation in the hippocampus: From magnesium to memory

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neuroscience 2024-11-29 Disease mechanisms

    Long-term potentiation (LTP) is a widely studied phenomenon since the underlying molecular mechanisms are widely believed to be critical for learning and memory and their dysregulation has been implicated in many brain disorders affecting cognitive functions.

  35. Amyloid-β Causes NMDA Receptor Dysfunction and Dendritic Spine Loss through mGluR1 and AKAP150-Anchored Calcineurin Signaling

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2024-09-11 Disease mechanisms

    Neuronal excitatory synapses are primarily located on small dendritic protrusions called spines.

  36. Mitigation of synaptic and memory impairments via F-actin stabilization in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer's research & therapy 2024-09-07 Disease mechanisms

    We found a significant reduction in PSD-95-actin association in synaptosomes from middle-aged APP/PS1 mice compared to wild-type (WT) mice.

  37. Cholesterol imbalance and neurotransmission defects in neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Experimental & molecular medicine 2024-08-01 Disease mechanisms

    The brain contains the highest concentration of cholesterol in the human body, which emphasizes the importance of cholesterol in brain physiology.

  38. A TrkB and TrkC partial agonist restores deficits in synaptic function and promotes activity-dependent synaptic and microglial transcriptomic changes in a late-stage Alzheimer's mouse model

    ✓ Peer-reviewed alzhub usefulness score 46 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2024-05-23 Disease mechanisms

    In APPL/S mice, BD10-2 treatment improved memory and LTP deficits.

  39. Alzheimer-like behavior and synaptic dysfunction in 3 × Tg-AD mice are reversed with calcineurin inhibition

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Experimental brain research 2024-05-08 Disease mechanisms

    Alzheimer's disease is a progressive neurodegenerative disorder characterized by impairments in synaptic plasticity and cognitive performance.

  40. Loss and microglia phagocytosis of synaptic proteins in frontotemporal lobar degeneration with TDP-43 proteinopathy

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurochemistry international 2024-03-05 Disease mechanisms

    Cortical synaptic loss has emerged as an early abnormality in Alzheimer's disease (AD) with a strong relationship to cognitive performance.

  41. Ketogenic diet and BHB rescue the fall of long-term potentiation in an Alzheimer's mouse model and stimulates synaptic plasticity pathway enzymes

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Communications biology 2024-02-16 Disease mechanisms

    The Ketogenic Diet (KD) improves memory and longevity in aged C57BL/6 mice.

  42. Synaptic Compensatory Plasticity in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2023-10-11 Disease mechanisms

    The loss of excitatory synapses is known to underlie the cognitive deficits in Alzheimer's disease (AD).

  43. Cdc42GAP deficiency contributes to the Alzheimer's disease phenotype

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain : a journal of neurology 2023-10-03 Disease mechanisms

    Alzheimer's disease, the most common cause of dementia, is a chronic degenerative disease with typical pathological features of extracellular senile plaques and intracellular neurofibrillary tangles and a significant decrease in the density of neuronal dendritic spines.

  44. Alzheimer risk-increasing TREM2 variant causes aberrant cortical synapse density and promotes network hyperexcitability in mouse models

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of disease 2023-08-15 TREM2 and immune genetics

    The R47H variant of triggering receptor expressed on myeloid cells 2 (TREM2) increases the risk of Alzheimer's disease (AD).

  45. The β-adrenergic hypothesis of synaptic and microglial impairment in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of neurochemistry 2023-02-28 Disease mechanisms

    Alzheimer's disease (AD) is a progressive neurodegenerative disease originating partly from amyloid β protein-induced synaptic failure.

  46. Presenilins regulate synaptic plasticity in the perforant pathways of the hippocampus

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Molecular brain 2023-01-30 Disease mechanisms

    Mutations in the Presenilin genes (PSEN1 and PSEN2) are the major cause of familial Alzheimer's disease (AD), highlighting the importance of Presenilin (PS) in AD pathogenesis.

  47. Jacob-induced transcriptional inactivation of CREB promotes Aβ-induced synapse loss in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. The EMBO journal 2023-01-03 Disease mechanisms

    Synaptic dysfunction caused by soluble β-amyloid peptide (Aβ) is a hallmark of early-stage Alzheimer's disease (AD), and is tightly linked to cognitive decline.

  48. miR-101a-3p Impairs Synaptic Plasticity and Contributes to Synucleinopathy

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Parkinson's disease 2023 Disease mechanisms

    We found several deregulated biological processes linked to the synapse. miR-101a-3p was validated as a synaptic miRNA upregulated in aSyn Tg mice and in the cortex of dementia with Lewy bodies patients.

  49. SNCA genetic lowering reveals differential cognitive function of alpha-synuclein dependent on sex

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Acta neuropathologica communications 2022-12-14 Drug development

    Antisense oligonucleotide (ASO) therapy for neurological disease has been successful in clinical settings and its potential has generated hope for Alzheimer's disease (AD).

  50. Amyloid β-Peptide Causes the Permanent Activation of CaMKIIα through Its Oxidation

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. International journal of molecular sciences 2022-12-02 Disease mechanisms

    Alzheimer's disease (AD) is characterised by the presence of extracellular amyloid plaques in the brain.

From across this tag

9 of the 287 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.

All topic tags with their study counts