Publications by authors named "Sagrario Manzano"
Introduction: Biomarker-informed criteria were proposed for the diagnosis of Alzheimer's disease (AD) by the National Institute on Aging and the Alzheimer's Association (NIA-AA) in 2011; however, the adequacy of this criteria has not been sufficiently evaluated.
Methods: ReDeMa () is a regional cohort of patients attending memory and neurology clinics. Core cerebrospinal fluid biomarkers were obtained, NIA-AA diagnostic criteria were considered, and changes in diagnosis and management were evaluated.
Article Synopsis
- Depression and anxiety are common in neurological disorders, significantly affecting patients' quality of life and disability levels, but they are often underdiagnosed and undertreated due to symptom complexity.
- Early identification and treatment of depression alongside neurological conditions are crucial to prevent worsening symptoms and increased disability.
- Treatment options exist, including medication and therapy, but their effectiveness can vary, leading to a need for collaborative care between neurologists and neuropsychiatry teams, especially in severe cases.
Alzheimer's disease (AD) is the most prevalent neurodegenerative condition, especially among elderly people. The presence of cortical β-amyloid deposition, together with tau phosphorylation and intracellular accumulation of neurofibrillary tangles (NFT) is the main neuropathologic criteria for AD diagnosis. Additionally, a role of inflammatory, mitochondrial, and metabolic factors has been suggested.
View Article and Find Full Text PDFBackground: Mild cognitive impairment (MCI) among an aging global population is a growing challenge for healthcare providers and payers. In many cases, MCI is an ominous portent for dementia. Early and accurate diagnosis of MCI provides a window of opportunity to improve the outcomes using a personalized care plan including lifestyle modifications to reduce the impact of modifiable risk factors (for example, blood pressure control and increased physical activity), cognitive training, dietary advice, and nutritional support.
View Article and Find Full Text PDFWe describe the clinical phenotype of nine kindred with presenile Alzheimer's disease (AD) caused by different presenilin 1 (PS1) point mutations, and compare them with reported families with mutations in the same codons. Mutations were in exon 4 (Phe105Val), exon 5 (Pro117Arg, Glu120Gly), exon 6 (His163Arg), exon 7 (Leu226Phe), exon 8 (Val261Leu, Val272Ala, Leu282Arg), and exon 12 (Ile439Ser). Three of these amino acid changes (Phe105Val, Glu120Gly, and Ile439Ser) had not been previously reported.
View Article and Find Full Text PDFBackground: Variability of age at onset (AO) of Alzheimer disease (AD) among members of the same family is important as a biological clue and because of its clinical effects.
Objective: To evaluate which clinical variables influence the discrepancy in AO among affected relatives with familial AD.
Setting: Clinical genetic project of Spanish kindred with AD conducted by 4 academic hospitals in Madrid, Spain.