Learning methods determine the degree of stimulation of engrams encoding information to be memorised. More enriching modes of learning allow more enduring long-term potentiation of the synapses associated with these memories. The additional activity causes a prolonged increase in [Ca2+] in the dendritic spine of the postsynaptic neuron. This allows Ca(2+)-mediated molecular pathways to bring about cytoskeletal remodeling, posttranslational modifications, and protein trafficking. These processes contribute to early long-term potentiation of the synapses, strengthening the memory they store and lead to improved performance on tests of memory recall.
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http://dx.doi.org/10.5214/ans.0972.7531.210408 | DOI Listing |
Biomaterials
January 2025
144 College St, Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, ON, M5S 3M2, Canada. Electronic address:
The development of disease-modifying therapeutics for Alzheimer's disease remains challenging due to the complex pathology and the presence of the blood-brain barrier. Previously we have described the investigation of a brain-penetrating multifunctional bioreactive nanoparticle system capable of remodeling the hypoxic and inflammatory brain microenvironment and reducing beta-amyloid plaques improving cognitive function in a mouse model of Alzheimer's disease. Despite the linkage of hypoxia and inflammation to metabolic alteration, the effects of this system on modulating cerebral glucose metabolism, mitochondrial activity and synaptic function remained to be elucidated.
View Article and Find Full Text PDFActa Neuropathol Commun
January 2025
Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Via Mario Negri 2, 20156, Milan, Italy.
Deposition of abnormally phosphorylated tau aggregates is a central event leading to neuronal dysfunction and death in Alzheimer's disease (AD) and other tauopathies. Among tau aggregates, oligomers (TauOs) are considered the most toxic. AD brains show significant increase in TauOs compared to healthy controls, their concentration correlating with the severity of cognitive deficits and disease progression.
View Article and Find Full Text PDFNeurochem Res
January 2025
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder characterized by cognitive decline. Despite extensive research, therapeutic options remain limited. Varenicline, an αβ nicotinic acetylcholine receptor agonist, shows promise in enhancing cognitive function.
View Article and Find Full Text PDFBrain Behav Immun Health
February 2025
Department of Physiology, School of Medicine, University College Cork, Western Road, Cork, Ireland.
Duchenne muscular dystrophy (DMD), an X-linked neuromuscular disorder, characterised by progressive immobility, chronic inflammation and premature death, is caused by the loss of the mechano-transducing signalling molecule, dystrophin. In non-contracting cells, such as neurons, dystrophin is likely to have a functional role in synaptic plasticity, anchoring post-synaptic receptors. Dystrophin-expressing hippocampal neurons are key to cognitive functions such as emotions, learning and the consolidation of memories.
View Article and Find Full Text PDFFront Neurosci
January 2025
Department of Neurophysiology, Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez", Mexico City, Mexico.
The interplay between long-term potentiation (LTP) and epilepsy represents a crucial facet in understanding synaptic plasticity and memory within neuroscience. LTP, a phenomenon characterized by a sustained increase in synaptic strength, is pivotal in learning and memory processes, particularly in the hippocampus. This review delves into the intricate relationship between LTP and epilepsy, exploring how alterations in synaptic plasticity mechanisms akin to those seen in LTP contribute to the hyperexcitable state of epilepsy.
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