Vascular cognitive impairment (VCI) is the second most common cause of cognitive deficit after Alzheimer's disease. Since VCI patients represent an important target population for prevention, an ongoing effort has been made to elucidate the pathogenesis of this disorder. In this review, we summarize the information from animal models on the molecular changes that occur in the brain during a cerebral vascular insult and ultimately lead to cognitive deficits in VCI. Animal models cannot effectively represent the complex clinical picture of VCI in humans. Nonetheless, they allow some understanding of the important molecular mechanisms leading to cognitive deficits. VCI may be caused by various mechanisms and metabolic pathways. The pathological mechanisms, in terms of cognitive deficits, may span from oxidative stress to vascular clearance of toxic waste products (such as amyloid beta) and from neuroinflammation to impaired function of microglia, astrocytes, pericytes, and endothelial cells. Impaired production of elements of the immune response, such as cytokines, and vascular factors, such as insulin-like growth factor 1 (IGF-1), may also affect cognitive functions. No single event could be seen as being the unique cause of cognitive deficits in VCI. These events are interconnected, and may produce cascade effects resulting in cognitive impairment.

• Keywords
• IGF-1, glial cells, neuroinflammation, oxidative stress, vascular cognitive impairment,
• MeSH
• Alzheimer Disease metabolism   MeSH
• Amyloid beta-Peptides metabolism   MeSH
• Astrocytes metabolism   MeSH
• Cytokines metabolism   MeSH
• Endothelial Cells metabolism   MeSH
• Insulin-Like Growth Factor I metabolism   MeSH
• Cognition * MeSH
• Cognitive Dysfunction metabolism   pathology   MeSH
• Humans MeSH
• Microglia metabolism   MeSH
• Models, Animal MeSH
• Brain metabolism   MeSH
• Nitric Oxide MeSH
• Oxidative Stress MeSH
• Pericytes metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Amyloid beta-Peptides MeSH
• Cytokines MeSH
• IGF1 protein, human MeSH Browser
• Insulin-Like Growth Factor I MeSH
• Nitric Oxide MeSH

Alzheimer's disease (AD) is a severe neurodegenerative disorder characterized by cognitive decline. Prodromal stage of AD, also called mild cognitive impairment (MCI), especially its amnestic type (aMCI), precedes dementia stage of AD. There are currently no reliable diagnostic biomarkers of AD in the blood. Alzheimer's disease is accompanied by increased oxidative stress in brain, which leads to oxidative damage and accumulation of free radical reaction end-products. In our study, specific products of lipid peroxidation in the blood of AD patients were studied. Lipophilic extracts of erythrocytes (AD dementia = 19, aMCI = 27, controls = 16) and plasma (AD dementia = 11, aMCI = 17, controls = 16) were analysed by fluorescence spectroscopy. The level of these products is significantly increased in erythrocytes and plasma of AD dementia and aMCI patients versus controls. We concluded that oxidative stress end-products are promising new biomarkers of AD, but further detailed characterisation of these products is needed.

• Keywords
• Alzheimer's disease, biomarkers, blood, lipofuscin-like pigments, oxidative stress,
• MeSH
• Alzheimer Disease blood   MeSH
• Erythrocytes metabolism   MeSH
• Spectrometry, Fluorescence MeSH
• Middle Aged MeSH
• Humans MeSH
• Lipids blood   MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Lipids MeSH