In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: Cognitive impairment is a common feature of late-life bipolar disorder (BD). Yet, there is limited information on the biological mechanisms associated with this process. It is uncertain whether cognitively impaired patients with BD may present the Alzheimer's disease (AD) bio-signature in the cerebrospinal fluid (CSF), defined as a combination of low concentrations of the amyloid-beta peptide (Aβ1-42 ) and high concentrations of total tau (T-tau) and tau phosphorylated at threonine 181 (P-tau). In this study, we sought to determine whether cognitive impairment in elderly patients with BD is associated with the AD CSF bio-signature.", 'Seventy-two participants were enrolled in the study. The test group comprised older adults with BD and mild cognitive impairment (BD-MCI; n\xa0=\xa016) and the comparison groups comprised patients with dementia due to AD (n\xa0=\xa017), patients with amnestic MCI (aMCI; n\xa0=\xa014), and cognitively healthy older adults (control group; n\xa0=\xa025). CSF samples were obtained by lumbar puncture and concentrations of Aβ1-42 , T-tau and P-tau were determined.', 'CSF concentrations of all biomarkers were significantly different in the AD group compared to all other groups, but did not differentiate BD-MCI subjects from aMCI subjects and controls. BD-MCI patients had a non-significant reduction in CSF Aβ1-42 compared to controls, but this was still higher than in the AD group. Concentrations of T-tau and P-tau in BD-MCI patients were similar to those in controls, and significantly lower than those in AD.\Question: Is cognitive impairment in late-life bipolar disorder associated with Alzheimer 's disease pathological signature in the cerebrospinal fluid?
Cognitively impaired patients with BD do not display the so-called AD bio-signature in the CSF. We therefore hypothesize that cognitive deterioration in BD is not associated with the classical pathophysiological mechanisms observed in AD, i.e., amyloid deposition and hyperphosphorylation of microtubule-associated tau protein.

Context: Information about malaria risk factors at high altitudes is scanty. Understanding the risk factors that determine the risk of malaria transmission at high altitude villages is important to facilitate implementing sustainable malaria control and prevention programs.', 'An unmatched case control study was conducted among patients seeking treatment at health centers in high altitude areas. Either microscopy or rapid diagnostic tests were used to confirm the presence of plasmodium species. A generalized linear model was used to identify the predictors of malaria transmission in high altitude villages.', 'Males (AOR\u200a=\u200a3.11, 95%CI: 2.28, 4.23), and those who traveled away from the home in the previous month (AOR\u200a=\u200a2.01, 95% CI: 1.56, 2.58) were strongly associated with presence of malaria in high altitude villages. Other significant factors, including agriculture in occupation (AOR\u200a=\u200a1.41, 95% CI: 1.05, 1.93), plants used for fencing (AOR\u200a=\u200a1.70, 95% CI: 1.18, 2.52) and forests near the house (AOR\u200a=\u200a1.60, 95% CI: 1.15, 2.47), were found predictors for malaria in high altitude villages.\Question: Are men traveling away from home more likely to bring malaria into high altitude villages , northwest Ethiopia?
Travel outside of their home was an important risk of malaria infections acquisition. Targeting males who frequently travel to malarious areas can reduce malaria transmission risks in high altitude areas.

Context: It is now well accepted that traumatic white matter injury constitutes a critical determinant of post-traumatic functional impairment. However, the contribution of preexisting white matter rarefaction on outcome following traumatic brain injury (TBI) is unknown. Hence, we sought to determine whether the burden of preexisting leukoaraiosis of presumed ischemic origin is independently associated with outcome after TBI.', 'We retrospectively analyzed consecutive, prospectively enrolled patients of ≥50\xa0years (n\xa0=\xa0136) who were admitted to a single neurological/trauma intensive care unit. Supratentorial white matter hypoattenuation on head CT was graded on a 5-point scale (range 0-4) reflecting increasing severity of leukoaraiosis. Outcome was ascertained according to the modified Rankin Scale (mRS) and Glasgow outcome scale (GOS) at 3 and 12\xa0months, respectively.', 'After adjustment for other factors, leukoaraiosis severity was significantly associated with a poor outcome at 3 and 12\xa0months defined as mRS 3-6 and GOS 1-3, respectively. The independent association between leukoaraiosis and poor outcome remained when the analysis was restricted to patients who survived up to 3\xa0months, had moderate-to-severe TBI [enrollment Glasgow Coma Scale (GCS) ≤12; p\xa0=\xa00.001], or had mild TBI (GCS 13-15; p\xa0=\xa00.002), respectively.\Question: Does severe leukoaraiosis portend a poor outcome after traumatic brain injury?

We provide first evidence that preexisting cerebral small vessel disease independently predicts a poor functional outcome after closed head TBI. This association is independent of other established outcome predictors such as age, comorbid state as well as intensive care unit complications and interventions. This knowledge may help improve prognostic accuracy, clinical management, and resource utilization.

