Difference in toxicity of β-amyloid peptide with aging in relation to nerve growth factor content in rat brain

Fukuta, Takanori; Nitta, Atsumi; Itoh, Akio; Furukawa, Shoei; Nabeshima, Toshitaka

doi:10.1007/s007020170090

Cited by 12 publications

(5 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Aging has been shown to render the brain more vulnerable to Aβ (Geula et al ., 1998; Fukuta et al ., 2001). Therefore, we investigated the effects of aging on the Aβ(1‐42)‐induced RPE damage.…”

Section: Resultsmentioning

confidence: 99%

Amyloid‐β(1‐42) alters structure and function of retinal pigmented epithelial cells

et al. 2009

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

Amyloid‐β(1‐42) alters structure and function of retinal pigmented epithelial cells

et al. 2009

View full text Add to dashboard Cite

“…Aβ(25–35) was administered i.c.v. to the rats in a single dose (10 μg) or via an osmotic minipump (Alzet) connected to a cannula implanted in the rat right lateral ventricle, as previously described (Nitta et al,1994; Ping Tang et al,2000; Fukuta et al,2001; Nag and Tang,2001). Chronic Aβ(25–35) or Aβ(35–25) infusion was carried out at a dose of 300 pmol/day for 14 days (Nag and Tang,2001).…”

Section: Methodsmentioning

confidence: 99%

Chronic but not acute intracerebroventricular administration of amyloid β‐peptide(25–35) decreases somatostatin content, adenylate cyclase activity, somatostatin‐induced inhibition of adenylate cyclase activity, and adenylate cyclase I levels in the rat hippocampus

Burgos‐Ramos

Hervás-Aguilar

Puebla‐Jiménez

et al. 2006

J of Neuroscience Research

View full text Add to dashboard Cite

Although alterations in adenylate cyclase (AC) activity and somatostatin (SRIF) receptor density have been reported in Alzheimer's disease, the effects of amyloid b-peptide (Ab) on these parameters in the hippocampus are unknown. Our aim was to investigate whether the peptide fragment Ab(25-35) can affect the somatostatinergic system in the rat hippocampus. Hence, Ab(25-35) was injected intracerebroventricularly (i.c.v.) to Wistar rats in a single dose or infused via an osmotic minipump connected to a cannula implanted in the right lateral ventricle during 14 days. The animals were decapitated 7 or 14 days after the single injection and 14 days after chronic infusion of the peptide. Chronic i.c.v. infusion of Ab(25-35) decreased SRIF-like immunoreactive content without modifying the SRIF receptor density, SRIF receptor expression, or the Gia 1 , Gia 2 , and Gia 3 protein levels in the hippocampus. This treatment, however, caused a decrease in basal and forskolin-stimulated AC activity as well as in the capacity of SRIF to inhibit AC activity. Furthermore, the protein levels of the neural-specific AC type I were significantly decreased in the hippocampus of the treated rats, whereas an increase in the levels of AC V/VI was found, with no alterations in type VIII AC. A single i.c.v. dose of Ab(25-35) exerted no effect on SRIF content or SRIF receptors but induced a slight decrease in forskolinstimulated AC activity and its inhibition by SRIF. Because chronic Ab(25-35) infusion impairs learning and memory whereas SRIF facilitates these functions, the alterations described here might be physiologically important given the decreased cognitive behavior previously reported in Ab-treated rats. V V C 2006 Wiley-Liss, Inc.

show abstract

“…[15][16][17][18] This is the first study to our knowledge examining the combined pathological and inflammatory effects of A␤ peptide-induced toxicity and ischemia in the rat. Previous investigations have shown that both acute and chronic injections of A␤(25-35) 19,20 and A␤(1-40) or A␤(1-42) [21][22][23] were neurotoxic; however, some questions remain unan- 6. A, Graphs of the results for the staircase test for the sham, endothelin, A␤, and A␤ and endothelin combined groups.…”

Section: Discussionmentioning

confidence: 99%

Interaction Between a Rat Model of Cerebral Ischemia and β-Amyloid Toxicity

Whitehead

Hachinski

Cechetto

2005

Stroke

View full text Add to dashboard Cite

Background and Purpose-Clinical data suggest that Alzheimer disease (AD) and stroke together potentiate cognitive impairment. Inflammatory mechanisms are involved in AD pathology and stroke and may be the mediator between AD and stroke toxicity. Methods-AD was modeled by cerebroventricular injections of ␤-amyloid (A␤ [25][26][27][28][29][30][31][32][33][34][35]) and subcortical lacunar infarcts by striatal endothelin injections. Inflammatory mechanisms were examined using immunohistochemical analysis. Memory and motor tasks were assessed using the Montoya staircase test. Results-A␤ injections elicited increases in pathological and inflammatory correlates of AD in multiple forebrain sites.Increases in astrocytosis and reactive microglia in the hippocampus were enhanced with the combination of endothelin and A␤ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)

show abstract

Difference in toxicity of β-amyloid peptide with aging in relation to nerve growth factor content in rat brain

Cited by 12 publications

References 38 publications

Amyloid‐β(1‐42) alters structure and function of retinal pigmented epithelial cells

Amyloid‐β(1‐42) alters structure and function of retinal pigmented epithelial cells

Chronic but not acute intracerebroventricular administration of amyloid β‐peptide(25–35) decreases somatostatin content, adenylate cyclase activity, somatostatin‐induced inhibition of adenylate cyclase activity, and adenylate cyclase I levels in the rat hippocampus

Interaction Between a Rat Model of Cerebral Ischemia and β-Amyloid Toxicity

Contact Info

Product

Resources

About