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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Silverberg, Gerald D Miller, Miles C Pascale, Crissey L Caralopoulos, Ilias N Agca, Yuksel Agca, Cansu Stopa, Edward G |
| Abstract | Background Normal pressure hydrocephalus (NPH) is most common in the elderly and has a high co-morbidity with Alzheimer’s disease (AD) and cerebrovascular disease (CVD). To understand the relationship between NPH, AD and CVD, we investigated how chronic hydrocephalus impacts brain amyloid-beta peptide (Aβ) accumulation and vascular pathology in an AD transgenic rodent model. Previously we showed that the altered CSF physiology produced by kaolin-hydrocephalus in older wild-type Sprague–Dawley rats increased Aβ and hyperphosphorylated Tau (Silverberg et. al. Brain Res. 2010, 1317:286–296). We postulated that hydrocephalus would similarly affect an AD rat model. Methods Thirty-five transgenic rats (tgAPP21) that express high levels of human APP and naturally overproduce Aβ40 were used. Six- (n = 7) and twelve-month-old (n = 9) rats had hydrocephalus induced by cisternal kaolin injection. We analyzed Aβ burden (Aβ40, Aβ42 and oligomeric Aβ) and vascular integrity (Masson trichrome and Verhoeff-Van Gieson) by immunohistochemistry and chemical staining at 10 weeks (n = 8) and 6 months (n = 5) post hydrocephalus induction. We also analyzed whether the vascular pathology seen in tgAPP21 rats, which develop amyloid angiopathy, was accelerated by hydrocephalus. Age-matched naïve and sham-operated tgAPP21 rats served as controls (n = 19). Results In hydrocephalic tgAPP21 rats, compared to naïve and sham-operated controls, there was increased Aβ 40 and oligomeric Aβ in hippocampal and cortical neurons at 10 weeks and 6 months post-hydrocephalus induction. No dense-core amyloid plaques were seen, but diffuse Aβ immunoreactivity was evident in neurons. Vascular pathology was accelerated by the induction of hydrocephalus compared to controls. In the six-month-old rats, subtle degenerative changes were noted in vessel walls at 10 weeks post-kaolin, whereas at six months post-kaolin and in the 12-month-old hydrocephalic rats more pronounced amyloid angiopathic changes were seen, with frequent large areas of infarction noted. Conclusions Kaolin-hydrocephalus can accelerate intraneuronal Aβ40 accumulation and vascular pathology in tgAPP21 rats. In addition, disrupted CSF production and reduced CSF turnover results in impaired Aβ clearance and accelerated vascular pathology in chronic hydrocephalus. The high co-morbidity seen in NPH, AD and CVD is likely not to be an age-related coincidence, but rather a convergence of pathologies related to diminished CSF clearance. |
| Related Links | https://fluidsbarrierscns.biomedcentral.com/counter/pdf/10.1186/2045-8118-12-2.pdf |
| Ending Page | 11 |
| Page Count | 11 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 20458118 |
| DOI | 10.1186/2045-8118-12-2 |
| Journal | Fluids and Barriers of the CNS |
| Issue Number | 1 |
| Volume Number | 12 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2015-01-24 |
| Access Restriction | Open |
| Subject Keyword | Neurosciences Hematology Neurobiology Normal pressure hydrocephalus Transgenic rat Kaolin-induced hydrocephalus Amyloid-beta peptide Cerebrovascular disease Amyloid angiopathy Solute clearance CSF circulation |
| Content Type | Text |
| Resource Type | Article |
| Subject | Neurology Developmental Neuroscience Medicine Cellular and Molecular Neuroscience |
| Journal Impact Factor | 5.9/2023 |
| 5-Year Journal Impact Factor | 7.5/2023 |
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