Cellular and metabolic alterations in the hippocampus caused by insulin signalling dysfunction and its association with cognitive impairment during aging and Alzheimer's disease: studies in animal models

2015 ◽  
Vol 31 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Erika Calvo-Ochoa ◽  
Clorinda Arias
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Animal Models ◽  
Insulin Signalling ◽  
Metabolic Alterations

Animal models of age-associated cognitive impairment of Alzheimer's disease

1994 ◽  
Vol 127 (1) ◽  
pp. 7
Author(s):  
Donald L. Price ◽  
Sangram S. Sisodia ◽  
Lee J. Martin ◽  
Lary C. Walker ◽  
Vassilis E. Koliatsos
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Animal Models

scholarly journals ACE2 activation protects against cognitive decline and reduces amyloid pathology in the Tg2576 mouse model of Alzheimer’s disease

2020 ◽  
Vol 139 (3) ◽  
pp. 485-502 ◽  
Author(s):  
Charles E. Evans ◽  
James S. Miners ◽  
Giulia Piva ◽  
Christine L. Willis ◽  
David M. Heard ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Animal Models ◽  
Cognitive Decline ◽  
Intraperitoneal Administration ◽  
Tg2576 Mouse ◽  
Model Of Alzheimer’S Disease ◽  
Increased Risk ◽  
Tg2576 Mice

Abstract Mid-life hypertension and cerebrovascular dysfunction are associated with increased risk of later life dementia, including Alzheimer’s disease (AD). The classical renin–angiotensin system (cRAS), a physiological regulator of blood pressure, functions independently within the brain and is overactive in AD. cRAS-targeting anti-hypertensive drugs are associated with reduced incidence of AD, delayed onset of cognitive decline, and reduced levels of Aβ and tau in both animal models and human pathological studies. cRAS activity is moderated by a downstream regulatory RAS pathway (rRAS), which is underactive in AD and is strongly associated with pathological hallmarks in human AD, and cognitive decline in animal models of CNS disease. We now show that enhancement of brain ACE2 activity, a major effector of rRAS, by intraperitoneal administration of diminazene aceturate (DIZE), an established activator of ACE2, lowered hippocampal Aβ and restored cognition in mid-aged (13–14-month-old) symptomatic Tg2576 mice. We confirmed that the protective effects of DIZE were directly mediated through ACE2 and were associated with reduced hippocampal soluble Aβ42 and IL1-β levels. DIZE restored hippocampal MasR levels in conjunction with increased NMDA NR2B and downstream ERK signalling expression in hippocampal synaptosomes from Tg2576 mice. Chronic (10 weeks) administration of DIZE to pre-symptomatic 9–10-month-old Tg2576 mice, and acute (10 days) treatment in cognitively impaired 12–13-month-old mice, prevented the development of cognitive impairment. Together these data demonstrate that ACE2 enhancement protects against and reverses amyloid-related hippocampal pathology and cognitive impairment in a preclinical model of AD.

scholarly journals Orally Administrated Cinnamon Extract Reduces β-Amyloid Oligomerization and Corrects Cognitive Impairment in Alzheimer's Disease Animal Models

PLoS ONE ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. e16564 ◽  
Author(s):  
Anat Frydman-Marom ◽  
Aviad Levin ◽  
Dorit Farfara ◽  
Tali Benromano ◽  
Roni Scherzer-Attali ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Animal Models ◽  
Cinnamon Extract ◽  
Β Amyloid
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