Background/Objectives: Norepinephrine (NE) plays a crucial role in modulating cognitive processes via α2A-adrenoceptors (α2A-ARs) within the prefrontal cortex (PFC), an essential brain region responsible for higher cognitive functions.
Yaru Wei +5 more
doaj +1 more source
Carbonic anhydrase inhibitor acetazolamide shifts synaptic vesicle recycling to a fast mode at the mouse neuromuscular junction [PDF]
Acetazolamide (AZ), a molecule frequently used to treat different neurological syndromes, is an inhibitor of the carbonic anhydrase (CA), an enzyme that regulates pH inside and outside cells.
Bertone Cueto, Nicolás Iván +5 more
core +1 more source
This study uncovers a new allosteric site in the Josephin domain of ataxin‐3 targeted by the molecular tweezer CLR01, which modulates protein aggregation, improves synaptic function in neuronal cells, and delays motor dysfunction in animal models.
Alexandra Silva +28 more
wiley +1 more source
Modifying Glucose Metabolism Reverses Memory Defects of Alzheimer's Disease Model at Late Stages
Using spatial transcriptomics, we show that ferul enanthate (SL‐ZF‐01) reverses episodic‐like memory deficits in aged, but not young, Alzheimer’s disease (AD) mice. SL restores glucose metabolism and Glucose Transporter 1/3 expression via an ‘Aging‐AD‐Rescue’ pattern, rescuing deficits seen in aged AD mice.
Fang Liu +14 more
wiley +1 more source
Presynaptic Boutons That Contain Mitochondria Are More Stable
The addition and removal of presynaptic terminals reconfigures neuronal circuits of the mammalian neocortex, but little is known about how this presynaptic structural plasticity is controlled.
Robert M. Lees +2 more
doaj +1 more source
The Alzheimer's β-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques. [PDF]
β-Site amyloid precursor protein (APP) cleaving enzyme-1 (BACE1) is the β-secretase that initiates Aβ production in Alzheimer's disease (AD). BACE1 levels are increased in AD, which could contribute to pathogenesis, yet the mechanism of BACE1 elevation is unclear. Furthermore, the normal function of BACE1 is poorly understood. We localized BACE1 in the
Kandalepas PC +5 more
europepmc +4 more sources
The binding of botulinum neurotoxins to different peripheral neurons [PDF]
Botulinum neurotoxins are the most potent toxins known. The double receptor binding modality represents one of the most significant properties of botulinum neurotoxins and largely accounts for their incredible potency and lethality.
Rossetto, O.
core +1 more source
Nanoscale Mapping of the Subcellular Glycosylation Landscape
Using multiplexed super‐resolution imaging with fluorophore‐labeled lectins, this study reports intracellular glycosylation at the nanoscale across organelles and synaptic specializations. Extending glycan analysis beyond the cell surface, Glyco‐STORM reveals distinct glycosylation nanodomains in the ER, Golgi, lysosomes, and synaptic sites.
Helene Gregoria Schroeter +4 more
wiley +1 more source
Conditional gene deletion reveals functional redundancy of GABAB receptors in peripheral nociceptors in vivo [PDF]
Background Gamma-aminobutyric acid (GABA) is an important inhibitory neurotransmitter which mainly mediates its effects on neurons via ionotropic (GABAA) and metabotropic (GABAB) receptors.
Bernhard Bettler +9 more
core +3 more sources
NDST3‐Induced Epigenetic Reprogramming Reverses Neurodegeneration in Parkinson's Disease
NDST3‐mediated epigenetic reprogramming revitalizes neuronal circuits in the substantia nigra and striatum to halt dopaminergic neuron degeneration and restore motor function in Parkinson's disease models. This strategy promotes neuronal maintenance and functional recovery, highlighting NDST3's therapeutic potential in neurodegenerative disorders ...
Yujung Chang +18 more
wiley +1 more source

