Results 261 to 270 of about 120,218 (348)
Abstract Aim Type 2 diabetes (T2D) is associated with increased dementia risk, but comparative data across newer glucose‐lowering therapies remain limited. We examined whether the initiation of GLP‐1 receptor agonists (GLP‐1 RAs) was associated with incident dementia compared with DPP4 inhibitors (DPP4is) and SGLT2 inhibitors (SGLT2is) in older adults ...
Ting Zhou +9 more
wiley +1 more source
The amyloid-beta wave hypothesis of Alzheimer's disease. [PDF]
Miller SJ, Logan R, Zhang C, Hafler BP.
europepmc +1 more source
Reducing the Levels of Akt Activation by PDK1 Knock-in Mutation Protects Neuronal Cultures against Synthetic Amyloid-Beta Peptides. [PDF]
Yang S +9 more
europepmc +1 more source
Amyloid-ß Acts as a regulator of neurotransmitter release disrupting the interaction between synaptophysin and VAMP2 [PDF]
Alifragis, P +5 more
core
Abstract Neurodegenerative diseases, including debilitating conditions like Alzheimer's and Parkinson's, are characterized by progressive neuronal loss, a process fundamentally driven by persistent chronic neuroinflammation and central metabolic dysfunction.
Renata Spezani +1 more
wiley +1 more source
Neuronal hyperexcitability: A key to unraveling hippocampal synaptic dysfunction in Lafora disease
Abstract Background and Objective Lafora disease (LD) is a rare progressive disorder caused by mutations in the EPM2A or EPM2B genes, characterized by the accumulation of Lafora bodies, drug‐resistant epilepsy, and cognitive decline. To investigate the early molecular mechanisms of LD, we studied electrophysiological changes in the dentate gyrus (DG ...
Cinzia Costa +17 more
wiley +1 more source
Redox environment modulates in vitro aggregation of Ataxin‐3, the protein implicated in spinocerebellar ataxia type 3. Reducing conditions stabilize native monomers and prevent aggregation, whereas oxidative conditions promote the formation of non‐native conformers and disulfide‐linked oligomers within the Josephin domain (JD).
Martyna Podlasiak +10 more
wiley +1 more source
A constant rate of DNA damage that is not perfectly repaired will cause a constant rate of DNA mutations. The chance of mutation will increase if DNA is prone to damage, such as occurs in somatic hypermutation (SHM) hotspots and GC‐rich DNA. Thus, if one mutation‐prone DNA site drives disease, the age of onset of disease and degree of penetrance should
Piet C. de Groen
wiley +1 more source

