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• W2472487575 abstract "The hippocampal CA2 area of the brain displays unique properties and connectivity that may be linked to disease. CA2 pyramidal neurons play a crucial role in the formation of social memory. Inhibitory neurons are highly concentrated in area CA2 and are uniquely altered in the hippocampus during several neurological disorders. The CA2 area is preferentially altered during schizophrenia and neurodegenerative diseases, and may be responsible, at least in part, for the social memory dysfunction phenotype in these diseases. While the hippocampus has long been recognized as a brain structure specialized in mapping ‘space’ in rodents, human studies and now recent data from rodents have shown that its function extends well beyond spatial coding. Recently, an overlooked area of the hippocampus, CA2, has emerged as a critical region for social memory. This area is also uniquely altered during several pathologies such as schizophrenia and age-related dementia. Because of its singular connectivity, we propose that area CA2 resides at the interface between emotional brain activity and higher cognitive function. Furthermore, because of the unique expression of multiple neuromodulator receptors in area CA2, we posit that this region may represent a fruitful therapeutic target for diseases where social dysfunction occurs. While the hippocampus has long been recognized as a brain structure specialized in mapping ‘space’ in rodents, human studies and now recent data from rodents have shown that its function extends well beyond spatial coding. Recently, an overlooked area of the hippocampus, CA2, has emerged as a critical region for social memory. This area is also uniquely altered during several pathologies such as schizophrenia and age-related dementia. Because of its singular connectivity, we propose that area CA2 resides at the interface between emotional brain activity and higher cognitive function. Furthermore, because of the unique expression of multiple neuromodulator receptors in area CA2, we posit that this region may represent a fruitful therapeutic target for diseases where social dysfunction occurs. a neurodegenerative disease resulting in memory impairments, impaired cognition, and dementia. a region of the limbic system and temporal lobe crucial for emotional behavior. extracellular aggregates of improperly folded proteins. proteolysis of this protein generates β-amyloid polypeptides, the main component of plaques found in Alzheimer's disease. a neurodegenerative disease in limbic structures characterized by dendritic projections detected by Golgi staining. a group of inherited neurodegenerative diseases characterized by accumulation of lipopigments in neurons, leading to blindness, epilepsy and cognitive impairments. a neurodegenerative disease characterized by cell loss in the cerebral cortex and basal ganglia, and resulting in motor deficits. abnormally shaped or swollen axons and dendrites, observed in neurodegenerative diseases. an elevated platform composed of open and enclosed arms. Based the inherent aversion of rodents to open spaces, the time spent in each region is indicative of anxiety. located in the medial temporal lobe, acts as a hub between the hippocampus and neocortex. temporal lobe brain structure of the limbic system, plays a central role in memory formation. potassium conductance that contributes to the resting membrane potential. neurodegenerative dementia affecting older adults that is characterized by the accumulation of α-synuclein protein within the cytoplasm of neurons. a lasting decrease in the strength of synaptic transmission as a result of synaptic plasticity. receptor of the nuclear receptor family with equal affinity for mineralocorticoids (e.g., aldosterone) and glucocorticoids (e.g., cortisol). intracellular aggregates of hyperphosphorylated tau protein observed during neurodegenerative diseases. the exogenous expression and illumination of opsins, channels activated by light, to rapidly excite neurons in a cell-selective manner. hypothalamic nucleus, source of oxytocin and vasopressin in the brain. neurodegenerative disorder affecting mainly the motor system. inhibitory synapses occurring around or near the soma of a neuron, controlling action potential firing. neurons displaying activity when an animal enters a particular location. neurodegenerative disease with neurofibrillary tangles associated with motor deficits and dementia. brainstem nuclei, major source of serotonin. transmissible spongiform encephalopathy affecting sheep and goats. set of nuclei reciprocally connected with numerous structures in the limbic system, thalamus, hypothalamus, and midbrain. May serve as a relay center linking reward and context. the ability to recognize novel versus familiar conspecifics, compromised in several neurological disorders. hypothalamic nucleus interconnected with several brain areas including the hippocampus. pathologies with disease-specific defects of tau protein. most common form of epilepsy characterized by recurrent seizures originating in the temporal lobe. rare progressive neurodegenerative disorders caused by infectious prion proteins. two-pore-domain potassium channels, contribute to leak current. a subtype of vasopressin receptor, this G protein-coupled receptor is scarce in the brain but is highly expressed in CA2." @default.
• W2472487575 created "2016-07-22" @default.
• W2472487575 creator A5012756347 @default.
• W2472487575 creator A5025045912 @default.
• W2472487575 date "2016-08-01" @default.
• W2472487575 modified "2023-10-13" @default.
• W2472487575 title "Hippocampal Area CA2: An Overlooked but Promising Therapeutic Target" @default.
• W2472487575 cites W1482320560 @default.
• W2472487575 cites W1487998758 @default.
• W2472487575 cites W1779226031 @default.
• W2472487575 cites W1846418424 @default.
• W2472487575 cites W1910377508 @default.
• W2472487575 cites W1965626594 @default.
• W2472487575 cites W1966790143 @default.
• W2472487575 cites W1967146781 @default.
• W2472487575 cites W1967982538 @default.
• W2472487575 cites W1976263707 @default.
• W2472487575 cites W1976913011 @default.
• W2472487575 cites W1979643175 @default.
• W2472487575 cites W1988075822 @default.
• W2472487575 cites W1992729034 @default.
• W2472487575 cites W1996254896 @default.
• W2472487575 cites W1999804106 @default.
• W2472487575 cites W2002728923 @default.
• W2472487575 cites W2006473457 @default.
• W2472487575 cites W2011504521 @default.
• W2472487575 cites W2013074165 @default.
• W2472487575 cites W2016652847 @default.
• W2472487575 cites W2018898953 @default.
• W2472487575 cites W2020972983 @default.
• W2472487575 cites W2021514539 @default.
• W2472487575 cites W2022245282 @default.
• W2472487575 cites W2023512898 @default.
• W2472487575 cites W2023775230 @default.
• W2472487575 cites W2024418933 @default.
• W2472487575 cites W2024495291 @default.
• W2472487575 cites W2025736222 @default.
• W2472487575 cites W2026686226 @default.
• W2472487575 cites W2027923831 @default.
• W2472487575 cites W2028274936 @default.
• W2472487575 cites W2031627377 @default.
• W2472487575 cites W2046897353 @default.
• W2472487575 cites W2047419237 @default.
• W2472487575 cites W2052515926 @default.
• W2472487575 cites W2056992784 @default.
• W2472487575 cites W2060196764 @default.
• W2472487575 cites W2065133826 @default.
• W2472487575 cites W2066256983 @default.
• W2472487575 cites W2066743763 @default.
• W2472487575 cites W2067117036 @default.
• W2472487575 cites W2067332645 @default.
• W2472487575 cites W2071678249 @default.
• W2472487575 cites W2078193966 @default.
• W2472487575 cites W2078446073 @default.
• W2472487575 cites W2079968698 @default.
• W2472487575 cites W2080044736 @default.
• W2472487575 cites W2081122323 @default.
• W2472487575 cites W2082406934 @default.
• W2472487575 cites W2082796074 @default.
• W2472487575 cites W2083205530 @default.
• W2472487575 cites W2084453479 @default.
• W2472487575 cites W2084681734 @default.
• W2472487575 cites W2087470227 @default.
• W2472487575 cites W2090594357 @default.
• W2472487575 cites W2094549516 @default.
• W2472487575 cites W2094954724 @default.
• W2472487575 cites W2095577856 @default.
• W2472487575 cites W2097436697 @default.
• W2472487575 cites W2098371930 @default.
• W2472487575 cites W2098403752 @default.
• W2472487575 cites W2102889249 @default.
• W2472487575 cites W2117023704 @default.
• W2472487575 cites W2119147856 @default.
• W2472487575 cites W2126338481 @default.
• W2472487575 cites W2129388256 @default.
• W2472487575 cites W2137036270 @default.
• W2472487575 cites W2145617691 @default.
• W2472487575 cites W2151173182 @default.
• W2472487575 cites W2154826398 @default.
• W2472487575 cites W2157402115 @default.
• W2472487575 cites W2164324272 @default.
• W2472487575 cites W2170097553 @default.
• W2472487575 cites W2170542996 @default.
• W2472487575 cites W2171865323 @default.
• W2472487575 cites W2179721010 @default.
• W2472487575 cites W2227829864 @default.
• W2472487575 cites W2229474614 @default.
• W2472487575 cites W2259382320 @default.
• W2472487575 cites W2288876215 @default.
• W2472487575 cites W2400693235 @default.
• W2472487575 cites W4253601648 @default.
• W2472487575 cites W80107653 @default.
• W2472487575 doi "https://doi.org/10.1016/j.molmed.2016.06.007" @default.
• W2472487575 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27372610" @default.
• W2472487575 hasPublicationYear "2016" @default.
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• W2472487575 citedByCount "53" @default.

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