3 research outputs found
The administration of federal Indian aid in the North-West Territories, 1879-1885
In 1879 the buffalo disappeared from the Canadian North-West, leaving the Plains Indians in an extreme state of destitution. In accordance with its treaty commitments to the Indians, the federal government undertook the responsibility of feeding the Indians of Treaties Four, Six and Seven. The government, in addition, introduced the reserve agricultural program, which it was hoped would transform the Indians into a self-supporting agrarian people. While the initial costs of rationing the Indians and assisting them in farming operations were high, it was hoped that within a few years the government would be largely relieved of such expenditures.In spite of the promising early returns made on reserves in the early 1880's the agricultural program did not succeed quickly enough to suit the government. One of the major reasons for the delay of the program was in fact the government's preoccupation with maintaining economy in Indian administration at all costs. When the government undertook a general reduction of expenditures on Indian administration in the North-West in 1833, any possibility of the reserve agricultural program succeeding was ended.The actions of various Indian bands and leaders in the North-West during these years were characterized by a desire to achieve suitable terms which would permit their people to make the transition to the farming way of life. The general cutbacks in spending introduced in 1883, however, sparked the formation of an Indian political movement seeking improved conditions. This movement grew rapidly, and likely would have unified Indians from all sections of the North-West in insisting upon the renegotiation of the treaties during the summer of 1885, had the Metis not rebelled. Although Indian participation in the North-West Uprising of 1885 was limited, it prompted the adoption of a policy of repression by the government in dealing with the Indians. The plan of assisting the Indians in becoming self-sufficient farmers was forgotten, and they became the charges of the Department of Indian Affairs
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A blood-based signature of cerebrospinal fluid A beta(1-42) status
It is increasingly recognized that Alzheimer's disease (AD) exists before dementia is present and that shifts in amyloid beta occur long before clinical symptoms can be detected. Early detection of these molecular changes is a key aspect for the success of interventions aimed at slowing down rates of cognitive decline. Recent evidence indicates that of the two established methods for measuring amyloid, a decrease in cerebrospinal fluid (CSF) amyloid beta(1-42) (A beta(1-42)) may be an earlier indicator of Alzheimer's disease risk than measures of amyloid obtained from Positron Emission Tomography (PET). However, CSF collection is highly invasive and expensive. In contrast, blood collection is routinely performed, minimally invasive and cheap. In this work, we develop a blood-based signature that can provide a cheap and minimally invasive estimation of an individual's CSF amyloid status using a machine learning approach. We show that a Random Forest model derived from plasma analytes can accurately predict subjects as having abnormal (low) CSF A beta(1-42) levels indicative of AD risk (0.84 AUC, 0.78 sensitivity, and 0.73 specificity). Refinement of the modeling indicates that only APOE epsilon 4 carrier status and four plasma analytes (CGA, A beta(1-42), Eotaxin 3, APOE) are required to achieve a high level of accuracy. Furthermore, we show across an independent validation cohort that individuals with predicted abnormal CSF A beta(1-42) levels transitioned to an AD diagnosis over 120 months significantly faster than those with predicted normal CSF A beta(1-42) levels and that the resulting model also validates reasonably across PET A beta(1-42) status (0.78 AUC). This is the first study to show that a machine learning approach, using plasma protein levels, age and APOE epsilon 4 carrier status, is able to predict CSF A beta(1-42) status, the earliest risk indicator for AD, with high accuracy
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Ferritin levels in the cerebrospinal fluid predict Alzheimer's disease outcomes and are regulated by APOE
Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study. Ferritin is the major iron storage protein of the body; by using cerebrospinal fluid (CSF) levels of ferritin as an index, we explored whether brain iron status impacts longitudinal outcomes in the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. We show that baseline CSF ferritin levels were negatively associated with cognitive performance over 7 years in 91 cognitively normal, 144 mild cognitive impairment (MCI) and 67 AD subjects, and predicted MCI conversion to AD. Ferritin was strongly associated with CSF apolipoprotein E levels and was elevated by the Alzheimer's risk allele, APOE-ɛ4. These findings reveal that elevated brain iron adversely impacts on AD progression, and introduce brain iron elevation as a possible mechanism for APOE-ɛ4 being the major genetic risk factor for AD