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John L. Dart Library
9 a.m. - 5 p.m.
Phone: (843) 722-7550
West Ashley Library
9 a.m. - 5 p.m.
Phone: (843) 766-6635
Folly Beach Library
9 a.m. - 2 p.m.
*open the 2nd and 4th Saturday
*open the 2nd and 4th Saturday
Phone: (843) 588-2001
Edgar Allan Poe/Sullivan's Island Library
Closed for renovations
Phone: (843) 883-3914
Wando Mount Pleasant Library
9 a.m. - 5 p.m.
Phone: (843) 805-6888
Village Library
9 a.m. - 1 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
9 a.m. - 5 p.m.
Phone: (843) 889-3300
Otranto Road Library
9 a.m. - 5 p.m.
Phone: (843) 572-4094
Mt. Pleasant Library
9 a.m. – 5 p.m.
Phone: (843) 849-6161
McClellanville Library
9 a.m. – 1 p.m.
Phone: (843) 887-3699
Keith Summey North Charleston Library
9 a.m. - 5 p.m.
Phone: (843) 744-2489
John's Island Library
9 a.m. - 5 p.m.
Phone: (843) 559-1945
Hurd/St. Andrews Library
9 a.m. - 5 p.m.
Phone: (843) 766-2546
Miss Jane's Building (Edisto Library Temporary Location)
9 a.m. – 1 p.m.
Phone: (843) 869-2355
Dorchester Road Library
9 a.m. - 5 p.m.
Phone: (843) 552-6466
Baxter-Patrick James Island
9 a.m. - 5 p.m.
Phone: (843) 795-6679
Main Library
9 a.m. - 5 p.m.
Phone: (843) 805-6930
Bees Ferry West Ashley Library
9 a.m. - 5 p.m.
Phone: (843) 805-6892
Mobile Library
Closed
Phone: (843) 805-6909
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Rodent Models of Alzheimer's Disease: Past Misconceptions and Future Prospects.
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- Author(s): Collins, Helen M.; Greenfield, Susan
- Source:
International Journal of Molecular Sciences; Jun2024, Vol. 25 Issue 11, p6222, 26p- Subject Terms:
- Source:
- Additional Information
- Abstract: Alzheimer's disease (AD) is a progressive neurodegenerative disease with no effective treatments, not least due to the lack of authentic animal models. Typically, rodent models recapitulate the effects but not causes of AD, such as cholinergic neuron loss: lesioning of cholinergic neurons mimics the cognitive decline reminiscent of AD but not its neuropathology. Alternative models rely on the overexpression of genes associated with familial AD, such as amyloid precursor protein, or have genetically amplified expression of mutant tau. Yet transgenic rodent models poorly replicate the neuropathogenesis and protein overexpression patterns of sporadic AD. Seeding rodents with amyloid or tau facilitates the formation of these pathologies but cannot account for their initial accumulation. Intracerebral infusion of proinflammatory agents offer an alternative model, but these fail to replicate the cause of AD. A novel model is therefore needed, perhaps similar to those used for Parkinson's disease, namely adult wildtype rodents with neuron-specific (dopaminergic) lesions within the same vulnerable brainstem nuclei, 'the isodendritic core', which are the first to degenerate in AD. Site-selective targeting of these nuclei in adult rodents may recapitulate the initial neurodegenerative processes in AD to faithfully mimic its pathogenesis and progression, ultimately leading to presymptomatic biomarkers and preventative therapies. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of International Journal of Molecular Sciences is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Abstract:
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