Higher levels of mid-life blood cholesterol level and blood cholesterol decline have been shown to increase risk for Alzheimer’s disease (AD). Our results confirm this finding.  Those who developed mild cognitive impairment and AD, had higher levels of blood cholesterol in mid-life and blood cholesterol decline prior to diagnosis.  A major risk gene for AD was not associated with these results.

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In the present study, we tested the effects of long-term consumption of a specific multi-nutrient diet in mice models for atherosclerosis and hypercholesterolemia. This specific multi-nutrient diet was developed to protect the membranes of neurons and stimulate formation of contacts (synapses) between neurons. The specific multi-nutrient diet decreased anxiety-related behavior and increased the concentration of omega-3 fatty acids in the brain. Furthermore, we found that mice fed with this multi-nutrient diet showed locally increased cerebral circulation. Together, these data suggest that a specific dietary intervention has beneficial effects on early cerebral pathological consequences of an impaired vascular system. 

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Overweight and obesity may increase risk for Alzheimer’s Disease (AD) and other dementias occurring in later life or after age 65 years Body Mass Index (BMI) is a common measure of overweight and obesity. BMI influences risk for dementia. Since BMI changes with age over the life course (increasing with increasing age during adult years, and decreasing with increasing age as one gets older) different dementia risk associations are observed in adulthood versus later life.  In midlife (to age 60 years), higher BMI increases risk for dementia. In late-life, higher BMI is protective for dementia.

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In this study we investigated the effect of apoE4, the main genetic risk factor for Alzheimer's disease, on the levels of two ApoE-receptors, Apoer2 and Lrp1 in different experimental paradigms. We showed that naïve apoE4 mice have decreased levels of the ApoE receptor, Apoer2, while activation of the amyloid cascade results in up-regulation of the ApoE receptor Lrp1. This study show that the levels of hippocampal ApoE receptors Lrp1 and Apoer2 in vivo are affected isoform specifically by ApoE4 and that the type of receptor affected is context dependent.

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Alzheimer’s disease has been the most frequent neurodegenerative disease with loss of memory. There are different animal models simulating the pathophysiological processes of Alzheimer’s disease. We used a rat model and found that injecting the toxic β-amyloid into the hippocampus caused simultaneous decrease of spatial memory and the number of synapses.

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