Neuroprotection in Cerebral Ischemia and Other Neurological Diseases

**127**

**1. Introduction**

**Chapter 7**

*In Vivo* Studies of

A Critical Review

*and Francisco Capani*

prevention of cognitive impairment.

**Abstract**

Protein Misfolding and

Neurodegeneration Induced by

Metabolic Syndrome Relative to

*María I. Herrera, Juan P. Luaces, Lucas D. Udovin,* 

*Nicolás Toro-Urrego, Matilde Otero-Losada* 

Chronic Cerebral Hypoperfusion:

Metabolic syndrome (MetS) leads to microvascular dysfunction and chronic cerebral hypoperfusion (CCH) in an insidious way. Clinical evidence and several rodent models have contributed to determining the neurodegenerative effect of a sustained decrease in cerebral blood flow (CBF). Protein misfolding and aggregation derived from CCH might account for the establishment of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). However, the complex and multifactorial etiology of cerebrovascular disease demands the

combination of experimental models in scientific research. In this sense, the present work aims at summarizing the differential available rodent paradigms for studying the establishment of cognitive decline resulting from protein misfolding induced by MetS in association with CCH. Revising experimental findings in the field will help further basic research on the pathophysiology of cerebrovascular disease and the future testing of protein-remodeling factors as neuroprotective agents for the

**Keywords:** metabolic syndrome (MetS), chronic cerebral hypoperfusion (CCH),

Metabolic syndrome (MetS) is the resulting condition of specific concurrent maladies, whose common pathogenic component is insulin resistance. Difficult to diagnose in clinical practice, there is consensus on its presence provided a cluster of risk factors be present, including abdominal obesity, hyperglycemia, hypertriglyceridemia, and hypertension [1–3]. Several murine models have contributed to

protein misfolding, experimental models, cognitive impairment
