FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2427946508> ?p ?o ?g. }

• W2427946508 abstract "Alzheimer´s disease is the most prevalent neurodegenerative disease, mostly idiopathic and with palliative treatment. Neuropathologically, it is characterized by intracellular neurofibrillary tangles of tau protein and extracellular plaques of amyloid β peptides. The relationship between Alzheimer’s disease and neurogenesis is unknown, but two facts are particularly relevant. First, early aggregation sites of both proteinopathies include the hippocampal formation and the olfactory bulb, which have been correlated to memory and olfactory deficits, respectively. These areas are well-recognized integration zones of newly-born neurons in the adult brain. Second, molecules, such as amyloid precursor protein and presenilin-1 are common to both Alzheimer’s disease etiology and neurogenic development. Adult neurogenesis in Alzheimer’s disease models has been studied in the hippocampus, but only occasionally addressed in the olfactory bulb and results are contradictory. To gain insight on the relationship between adult neurogenesis and Alzheimer’s disease, this work analyzes neurogenesis, neurodegeneration, interneuron vulnerability and amyloid-β involvement in the olfactory bulb of an Alzheimer’s disease model. Control and double-transgenic mice carrying the amyloid precursor protein and the presenilin-1 genes, which give rise amyloid β plaques have been used. BrdU-treated animals have been studied at 16, 30, 43 and 56 weeks of age. New-born cell survival (BrdU), neuronal loss (using neuronal markers NeuN and PGP9.5), differential interneuron (calbindin-, parvalbumin-, calretinin- and somatostatin-expressing populations) vulnerability and involvement by amyloid β have been analyzed. Neurogenesis increases with aging in the granule cell layer of control animals from 16 to 43 weeks. No neuronal loss has been observed after quantifying NeuN or PGP9.5. Regarding interneuron population vulnerability: calbindin-expressing neurons remains unchanged; parvalbumin-expressing neurons trend to increase with aging in transgenic animals; calretinin-expressing neurons increase with aging in transgenic mice and decrease in control animals and neurogenesis is higher in control as compared to transgenic animals at given ages, finally; somatostatin-expressing neurons of transgenic mice decrease with aging and as compared to controls. Amyloid β aggregates with aging in the granule cell layer, which may be related to the particular involvement of somatostatin-expressing cells." @default.
• W2427946508 created "2016-06-24" @default.
• W2427946508 creator A5018106052 @default.
• W2427946508 creator A5019918561 @default.
• W2427946508 creator A5029506591 @default.
• W2427946508 creator A5033585543 @default.
• W2427946508 creator A5068403643 @default.
• W2427946508 date "2016-05-30" @default.
• W2427946508 modified "2023-10-18" @default.
• W2427946508 title "Neurogenesis, Neurodegeneration, Interneuron Vulnerability, and Amyloid-β in the Olfactory Bulb of APP/PS1 Mouse Model of Alzheimer's Disease" @default.
• W2427946508 cites W1509173389 @default.
• W2427946508 cites W1510052211 @default.
• W2427946508 cites W1527739960 @default.
• W2427946508 cites W1577915886 @default.
• W2427946508 cites W1965058371 @default.
• W2427946508 cites W1965792394 @default.
• W2427946508 cites W1968453815 @default.
• W2427946508 cites W1968840425 @default.
• W2427946508 cites W1972960028 @default.
• W2427946508 cites W1975141413 @default.
• W2427946508 cites W1977547378 @default.
• W2427946508 cites W1980225806 @default.
• W2427946508 cites W1980499453 @default.
• W2427946508 cites W1980550586 @default.
• W2427946508 cites W1983456059 @default.
• W2427946508 cites W1990469555 @default.
• W2427946508 cites W1991405782 @default.
• W2427946508 cites W1995142957 @default.
• W2427946508 cites W1996018734 @default.
• W2427946508 cites W1996649428 @default.
• W2427946508 cites W1996730507 @default.
• W2427946508 cites W2003278562 @default.
• W2427946508 cites W2007242343 @default.
• W2427946508 cites W2008803278 @default.
• W2427946508 cites W2010773967 @default.
• W2427946508 cites W2012511275 @default.
• W2427946508 cites W2015708455 @default.
• W2427946508 cites W2019427919 @default.
• W2427946508 cites W2022348989 @default.
• W2427946508 cites W2024601402 @default.
• W2427946508 cites W2025246895 @default.
• W2427946508 cites W2026393786 @default.
• W2427946508 cites W2035250926 @default.
• W2427946508 cites W2039069312 @default.
• W2427946508 cites W2044700058 @default.
• W2427946508 cites W2052742260 @default.
• W2427946508 cites W2057048975 @default.
• W2427946508 cites W2057496129 @default.
• W2427946508 cites W2067616890 @default.
• W2427946508 cites W2067668823 @default.
• W2427946508 cites W2081016744 @default.
• W2427946508 cites W2082796074 @default.
• W2427946508 cites W2085760151 @default.
• W2427946508 cites W2088033629 @default.
• W2427946508 cites W2092512185 @default.
• W2427946508 cites W2093650784 @default.
• W2427946508 cites W2100211448 @default.
• W2427946508 cites W2102799749 @default.
• W2427946508 cites W2105176976 @default.
• W2427946508 cites W2105499841 @default.
• W2427946508 cites W2115290127 @default.
• W2427946508 cites W2128527975 @default.
• W2427946508 cites W2141535241 @default.
• W2427946508 cites W2142277081 @default.
• W2427946508 cites W2144749167 @default.
• W2427946508 cites W2145796722 @default.
• W2427946508 cites W2151761943 @default.
• W2427946508 cites W2156297351 @default.
• W2427946508 cites W2162462376 @default.
• W2427946508 cites W2162798214 @default.
• W2427946508 cites W2196832857 @default.
• W2427946508 cites W2386517867 @default.
• W2427946508 cites W2946976245 @default.
• W2427946508 cites W3023013291 @default.
• W2427946508 cites W610927360 @default.
• W2427946508 doi "https://doi.org/10.3389/fnins.2016.00227" @default.
• W2427946508 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4885141" @default.
• W2427946508 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27303258" @default.
• W2427946508 hasPublicationYear "2016" @default.
• W2427946508 type Work @default.
• W2427946508 sameAs 2427946508 @default.
• W2427946508 citedByCount "17" @default.
• W2427946508 countsByYear W24279465082017 @default.
• W2427946508 countsByYear W24279465082018 @default.
• W2427946508 countsByYear W24279465082019 @default.
• W2427946508 countsByYear W24279465082020 @default.
• W2427946508 countsByYear W24279465082021 @default.
• W2427946508 countsByYear W24279465082022 @default.
• W2427946508 crossrefType "journal-article" @default.
• W2427946508 hasAuthorship W2427946508A5018106052 @default.
• W2427946508 hasAuthorship W2427946508A5019918561 @default.
• W2427946508 hasAuthorship W2427946508A5029506591 @default.
• W2427946508 hasAuthorship W2427946508A5033585543 @default.
• W2427946508 hasAuthorship W2427946508A5068403643 @default.
• W2427946508 hasBestOaLocation W24279465081 @default.
• W2427946508 hasConcept C142724271 @default.
• W2427946508 hasConcept C148762608 @default.
• W2427946508 hasConcept C169760540 @default.
• W2427946508 hasConcept C17077164 @default.
• W2427946508 hasConcept C175344181 @default.

• next