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• W2339935211 abstract "English Alzheimer’s disease (AD) and vascular dementia (VaD) are currently considered the most common dementia forms. They are usually approached separately, and much research is focused on identifying means to differentiate one from the other. However, evidence has accumulated during the past years that there is considerable overlap between AD and VaD in terms of clinical symptoms, neuropathology and risk factors, and that vascular factors are important not only for VaD but also for AD. The aim of the present project is to investigate the relations between late-life cognition, dementia, AD, VaD and cholesterol metabolism in a more integrative way, by combining an epidemiological with a clinic-based approach, and by addressing both peripheral and brain cholesterol homeostasis. The epidemiological part is based on data on serum total cholesterol from a prospective 21-year follow-up cohort study in a Finnish population (Cardiovascular Risk Factors, Aging and Incidence of Dementia, CAIDE) and a retrospective 30-year follow-up cohort study in a multiethnic USA population (Kaiser Permanente of Northern California). Clinicbased studies were conducted at Karolinska University Hospital, Huddinge, Sweden, and focus on CSF markers of cholesterol homeostasis (total cholesterol, 24and 27-hydroxycholesterol, apolipoprotein E) and the relations between serum markers of cholesterol homeostasis (total cholesterol, LDL, HDL, 24and 27hydroxycholesterol, lathosterol, and lanosterol) and brain volumes (white matter, gray matter, CSF, and total intracranial volume; parenchymal, white matter, gray matter and CSF fractions) in patients with subjective cognitive impairment (SCI), mild cognitive impairment (MCI) and AD. The results of the project confirm the existence of a relation between cholesterol and AD as well as VaD. High serum total cholesterol at midlife consistently emerged as a risk factor for late-life dementia or cognitive impairment or poorer performance in cognitive tests. However, the significance of serum cholesterol at older ages turned out to be less straightforward. In epidemiological studies, late-life cholesterol did not appear to be related to cognition. Cholesterol levels decreased over time in most individuals, and especially in those who developed dementia or cognitive impairment. A decrease in cholesterol from midlife to late-life was significantly associated with increased risk of having a more impaired late-life cognitive status, even after adjusting for a wide range of confounders. This association was not significant in statin users. In clinical studies, patients with AD had lower serum levels of the cholesterol precursors lathosterol and lanosterol, and of 27-hydroxycholesterol compared to patients with MCI or SCI, suggestive of a possible disturbance in cholesterol homeostasis with decreased cholesterol synthesis. Also, lower totaland LDL-cholesterol were significantly related to lower brain volumes/higher CSF volumes in patients with AD, but not with MCI or SCI. On the contrary, in persons with SCI (but not AD or MCI) there was an inverse association between lathosterol, lanosterol and brain volumes (lower levels of cholesterol precursors related to higher brain volumes/lower CSF volumes). These patterns seem to indicate a central nervous system (CNS) induced effect of disease on extracerebral cholesterol homeostasis. A window into brain cholesterol metabolism was provided by CSF analyses. The relations found between 24hydroxycholesterol (24OHC) and apolipoprotein E (apoE) levels in patients with AD and MCI (but not controls) indicate a role for the 24OHC-apoE system in the regulation and control of neurodegeneration, suggesting that the 24OHC-mediated secretion of apoE creates an overcapacity for transport of steroids from the CNS under conditions of neurodegeneration (when dying neuronal cells lead to increased levels of free cholesterol) but not under normal conditions. Patients with AD had the highest 24OHC levels in CSF and the lowest 24OHC levels in serum. Moreover, serum 24OHC was related to gray matter measurements. Thus, 24OHC levels in serum could function as a marker of the number of metabolically active neurons, while 24OHC in CSF may instead reflect neuronal damage and rate of neuronal loss. These results point out the importance of shifting the focus from the extreme category of dementia as a late-life event to a life-long view of pathological processes influencing cognition. Cholesterol is among the modifiable risk factors that can be targeted by preventive strategies already at midlife. However, serum cholesterol levels may be influenced by the very disease(s) it contributes to; at older ages, circulating cholesterol may instead become a reflection of ongoing pathological processes in the brain. Further studies are needed to investigate the usefulness of markers of brain cholesterol metabolism in diagnosing the cause(s) of cognitive impairment and in monitoring disease progression. National Library of Medicine Classification: WT 155, QU 95 Medical Subject Headings:Alzheimer Disease/preventionc Alzheimer Disease/epidemiology; Dementia, Vascular/epidemiology; Age Factors; Brain; Cholesterol; Homeostasis; Hydroxycholesterols; Risk Factors; Biological Markers; Apolipoprotein E; Lanosterol; Cerebrospinal Fluid; Longitudinal Studies" @default.
• W2339935211 created "2016-06-24" @default.
• W2339935211 creator A5086456642 @default.
• W2339935211 date "2009-01-01" @default.
• W2339935211 modified "2023-09-26" @default.
• W2339935211 title "Cholesterol and late-life cognition. An epidemiological and clinical approach" @default.
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