Pages that link to "Q30495675"
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The following pages link to Co-occurrence of Alzheimer's disease ß-amyloid and τ pathologies at synapses. (Q30495675):
Displaying 50 items.
- Role of pro-inflammatory cytokines released from microglia in Alzheimer's disease (Q26799870) (← links)
- Intraneuronal Aβ accumulation induces hippocampal neuron hyperexcitability through A-type K( ) current inhibition mediated by activation of caspases and GSK-3. (Q27307787) (← links)
- Analyzing dendritic spine pathology in Alzheimer's disease: problems and opportunities (Q28087158) (← links)
- Synaptic protein α1-takusan mitigates amyloid-β-induced synaptic loss via interaction with tau and postsynaptic density-95 at postsynaptic sites (Q28577234) (← links)
- Synaptic activity reduces intraneuronal Abeta, promotes APP transport to synapses, and protects against Abeta-related synaptic alterations (Q30491040) (← links)
- Effects of synaptic modulation on beta-amyloid, synaptophysin, and memory performance in Alzheimer's disease transgenic mice. (Q30497246) (← links)
- Neuroprotection by IFN-γ via astrocyte-secreted IL-6 in acute neuroinflammation (Q32178128) (← links)
- MEG Beamformer-Based Reconstructions of Functional Networks in Mild Cognitive Impairment (Q33600113) (← links)
- Computational study of hippocampal-septal theta rhythm changes due to β-amyloid-altered ionic channels (Q33948010) (← links)
- Synapses, synaptic activity and intraneuronal abeta in Alzheimer's disease (Q34028039) (← links)
- Inducing Autophagy by Rapamycin Before, but Not After, the Formation of Plaques and Tangles Ameliorates Cognitive Deficits (Q34043165) (← links)
- Oligomeric Aβ-induced synaptic dysfunction in Alzheimer's disease (Q34544243) (← links)
- Accumulation of intraneuronal β-amyloid 42 peptides is associated with early changes in microtubule-associated protein 2 in neurites and synapses (Q34570846) (← links)
- Single-subject grey matter graphs in Alzheimer's disease (Q34639435) (← links)
- αν and β1 Integrins mediate Aβ-induced neurotoxicity in hippocampal neurons via the FAK signaling pathway (Q34765883) (← links)
- Synaptic change in the posterior cingulate gyrus in the progression of Alzheimer's disease (Q35035669) (← links)
- Abnormal tau, mitochondrial dysfunction, impaired axonal transport of mitochondria, and synaptic deprivation in Alzheimer's disease (Q35223831) (← links)
- AD synapses contain abundant Aβ monomer and multiple soluble oligomers, including a 56-kDa assembly (Q35353667) (← links)
- Graph theoretic analysis of structural connectivity across the spectrum of Alzheimer's disease: The importance of graph creation methods (Q35598903) (← links)
- Involvement of Intracellular and Mitochondrial Aβ in the Ameliorative Effects of Huperzine A against Oligomeric Aβ42-Induced Injury in Primary Rat Neurons (Q35646336) (← links)
- Isolation of synaptic terminals from Alzheimer's disease cortex (Q35860859) (← links)
- Alzheimer's disease: a clinical practice-oriented review (Q35899503) (← links)
- Extensive p-tau pathology and SDS-stable p-tau oligomers in Alzheimer's cortical synapses (Q36137237) (← links)
- Critical role of intraneuronal Aβ in Alzheimer's disease: technical challenges in studying intracellular Aβ. (Q36342011) (← links)
- Synaptic Amyloid-β Oligomers Precede p-Tau and Differentiate High Pathology Control Cases (Q36468755) (← links)
- Development of new fusion proteins for visualizing amyloid-β oligomers in vivo (Q36691716) (← links)
- Blocking the interaction between apolipoprotein E and Aβ reduces intraneuronal accumulation of Aβ and inhibits synaptic degeneration (Q36817618) (← links)
- Oxidative stress and hippocampal synaptic protein levels in elderly cognitively intact individuals with Alzheimer's disease pathology (Q36873070) (← links)
- Abnormal interaction of oligomeric amyloid-β with phosphorylated tau: implications to synaptic dysfunction and neuronal damage (Q37618817) (← links)
- Tau protein modifications and interactions: their role in function and dysfunction (Q37684106) (← links)
- Interaction between pathogenic proteins in neurodegenerative disorders (Q37969262) (← links)
- Microglia receptors and their implications in the response to amyloid β for Alzheimer's disease pathogenesis (Q38195641) (← links)
- Glia and zinc in ageing and Alzheimer's disease: a mechanism for cognitive decline? (Q38227862) (← links)
- Neuropathology and biochemistry of Aβ and its aggregates in Alzheimer's disease. (Q38297925) (← links)
- Cellular factors modulating the mechanism of tau protein aggregation (Q38350075) (← links)
- Alzheimer's Disease, Drosophila melanogaster and Polyphenols. (Q38532705) (← links)
- Overexpression of Heme Oxygenase 1 Impairs Cognitive Ability and Changes the Plasticity of the Synapse (Q38832929) (← links)
- Recent publications from the Alzheimer's Disease Neuroimaging Initiative: Reviewing progress toward improved AD clinical trials. (Q38876654) (← links)
- Plaque formation and the intraneuronal accumulation of β-amyloid in Alzheimer's disease (Q39163007) (← links)
- Interactions of pathological proteins in neurodegenerative diseases (Q39236779) (← links)
- Selective impairment of hippocampus and posterior hub areas in Alzheimer's disease: an MEG-based multiplex network study (Q40277605) (← links)
- Pseudo-acetylation of multiple sites on human Tau proteins alters Tau phosphorylation and microtubule binding, and ameliorates amyloid beta toxicity (Q41564705) (← links)
- Impaired plasticity of cortical dendritic spines in P301S tau transgenic mice (Q41849339) (← links)
- Heterogeneous Association of Alzheimer's Disease-Linked Amyloid-β and Amyloid-β Protein Precursor with Synapses (Q42219931) (← links)
- Intracellular accumulation of amyloid-β (Aβ) protein plays a major role in Aβ-induced alterations of glutamatergic synaptic transmission and plasticity. (Q42465835) (← links)
- Memantine for the Treatment of Dementia: A Review on its Current and Future Applications. (Q47280369) (← links)
- Beta-amyloid induced changes in A-type K⁺ current can alter hippocampo-septal network dynamics. (Q48884122) (← links)
- AD-Related N-Terminal Truncated Tau Is Sufficient to Recapitulate In Vivo the Early Perturbations of Human Neuropathology: Implications for Immunotherapy (Q50420723) (← links)
- Synaptic Dysfunction in Alzheimer's Disease: Aβ, Tau, and Epigenetic Alterations. (Q50440796) (← links)
- The γ-secretase modulator CHF5074 reduces the accumulation of native hyperphosphorylated tau in a transgenic mouse model of Alzheimer's disease (Q51026158) (← links)