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Ying Jiang,Kuldeep Sachdeva,Chris N Goulbourne et al. Ying Jiang et al.
Endosomal system dysfunction within neurons is a prominent early feature of Alzheimer's disease (AD) pathology. Multiple AD risk factors are regulators of endocytosis and are known to cause hyper-activity of the early-endosome small GTPase ...
Gabriele Tancreda,Silvia Ravera,Isabella Panfoli Gabriele Tancreda
Recognized AD pathological hallmarks include amyloid beta plaque and neurofibrillary tangle formation, synaptic dysfunction with considerable apoptosis of cholinergic and dopaminergic neurons, and high levels of oxidative stress and neuroinflammation.
Elena Popa,Andrei Emilian Popa,Mihaela Poroch et al. Elena Popa et al.
Microglial activation and cytokine release (e.g., IL-6, TNF-α) promote synaptic dysfunction and neuronal injury, while activation of inflammasomes such as NLRP3 amplifies CNS inflammation.
Dehui Kong,Hongjie He,Joseph Lechner et al. Dehui Kong et al.
These alterations were associated with AD-related pathways, including neuroinflammation and immune dysregulation, and synaptic dysfunction and neuronal signaling in microglia, as well as lysosomal and proteasomal activity, lipoprotein metabolism, and mitochondrial dysfunction in astrocytes.
Fenglian Xu,Zijun Liu,Ziyu Wang et al. Fenglian Xu et al.
Recent studies have shown that p53 regulates pathological processes such as apoptosis, ferroptosis, neuroinflammation, mitochondrial dysfunction, DNA damage, and synaptic dysfunction through complex molecular pathways.
Şişman Büşra Aysel,Savaş Merve,Koral Gizem et al. Şişman Büşra Aysel et al.
Background and purpose: The role of synaptic dysfunction in focal epilepsy of unknown cause is not well understood.
Susmita Malwade,Carl M Sellgren,Navneet A Vasistha et al. Susmita Malwade et al.
Group A CNVs were associated with synaptic signaling, suggesting that synaptic dysfunction observed in NDDs may originate very early during fetal brain development. Group B CNVs were related to cell cycle and suggest dysfunction in proliferation and differentiation of precursor cells.
Elizabeth M Planalp,Rebecca E Langhough,Erin M Jonaitis et al. Elizabeth M Planalp et al.
Moreover, a SNAP-25/NPTX2 ratio of synaptic dysfunction explained more variance in cognitive decline than other biomarkers alone.
Nadine Alshakhshir,Lucy He,Liqin Zhao Nadine Alshakhshir
We hypothesize that these molecular changes can be a shared mechanistic contributor to synaptic dysfunction in AD and diabetes.
Barbora Fulopova,William Bennett,Alison J Canty Barbora Fulopova
Aim: As synaptic dysfunction is one of the key mechanisms associated with cognitive deficits in dementia, we investigated the effect of rTMS on cortical synapses using an APP/PS1 amyloidosis mouse model of AD crossed with fluorescent reporters linked to the Thy-1 promoter.
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