Lancet neurology
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We have previously characterised functional brain abnormalities in young adults at genetic risk for late-onset Alzheimer's disease. To gain further knowledge on the preclinical phase of Alzheimer's disease, we sought to characterise structural and functional MRI, CSF, and plasma biomarkers in a cohort of young adults carrying a high-penetrance autosomal dominant mutation that causes early-onset Alzheimer's disease. ⋯ Banner Alzheimer's Foundation, Nomis Foundation, Anonymous Foundation, Forget Me Not Initiative, Boston University Department of Psychology, Colciencias, National Institute on Aging, National Institute of Neurological Disorders and Stroke, and the State of Arizona.
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Previous studies have identified effects of age and vascular risk factors on brain injury in elderly individuals. We aimed to establish whether the effects of high blood pressure in the brain are evident as early as the fifth decade of life. ⋯ National Institutes of Health and National Heart, Lung, and Blood Institute; National Institute on Aging; and National Institute of Neurological Disorders and Stroke.
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Fibrillar amyloid-β (Aβ) is thought to begin accumulating in the brain many years before the onset of clinical impairment in patients with Alzheimer's disease. By assessing the accumulation of Aβ in people at risk of genetic forms of Alzheimer's disease, we can identify how early preclinical changes start in individuals certain to develop dementia later in life. We sought to characterise the age-related accumulation of Aβ deposition in presenilin 1 (PSEN1) E280A mutation carriers across the spectrum of preclinical disease. ⋯ Avid Radiopharmaceuticals, Banner Alzheimer's Foundation, Nomis Foundation, Anonymous Foundation, Forget Me Not Initiative, Colciencias, National Institute on Aging, and the State of Arizona.
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People with epilepsy have a high risk of developing depressive disorders, and people with primary depressive disorders have a high risk of developing epilepsy. Furthermore, a lifetime history of depressive disorders has been associated with a poor response of the seizure disorder to pharmacotherapy and epilepsy surgery. ⋯ These mechanisms include (1) a hyperactive hypothalamic-pituitary-adrenal axis; (2) structural and functional abnormalities of cortical structures; (3) increased glutamatergic and decreased GABAergic and serotonergic activity; and (4) immunological abnormalities. The data presented in this Review provide experimental evidence that might begin to explain the bidirectional relation between depressive disorders and epilepsy and that can be regarded as a source for future research.