The Experts below are selected from a list of 15 Experts worldwide ranked by ideXlab platform

Alan Mcgregor - One of the best experts on this subject based on the ideXlab platform.

  • association between autoimmune thyroid Disease and Familial Alzheimers Disease
    Clinical Endocrinology, 1991
    Co-Authors: Dl Ewins, Martin N Rossor, J Butler, P Roques, Michael Mullan, Alan Mcgregor
    Abstract:

    OBJECTIVE: To determine the prevalence of autoimmune thyroid Disease in Familial Alzheimer's Disease kindreds and to ascertain whether there is any evidence for genetic linkage between the two conditions. DESIGN: Retrospective study of Familial Alzheimer's Disease kindreds. PATIENTS: Seventy affected and unaffected family members from 12 kindreds. MEASUREMENTS: Anti-thyroglobulin and anti-microsomal autoantibody status was determined using an enzyme-linked immunosorbent assay. Thyrotrophin levels were determined by an immunoradiometric assay. RESULTS: Of the family members, 41.4% had evidence of autoimmune thyroid Disease, with significant co-segregation between the presence of thyroid autoantibodies and the development of Alzheimer's Disease (P less than 0.01). CONCLUSIONS: This study demonstrates a very high prevalence of autoimmune thyroid Disease in Familial Alzheimer's Disease kindreds and suggests that a genetic factor contributing towards the development of autoimmune thyroid Disease may be located on chromosome 21 within close proximity to the Familial Alzheimer's Disease gene.

Dl Ewins - One of the best experts on this subject based on the ideXlab platform.

  • association between autoimmune thyroid Disease and Familial Alzheimers Disease
    Clinical Endocrinology, 1991
    Co-Authors: Dl Ewins, Martin N Rossor, J Butler, P Roques, Michael Mullan, Alan Mcgregor
    Abstract:

    OBJECTIVE: To determine the prevalence of autoimmune thyroid Disease in Familial Alzheimer's Disease kindreds and to ascertain whether there is any evidence for genetic linkage between the two conditions. DESIGN: Retrospective study of Familial Alzheimer's Disease kindreds. PATIENTS: Seventy affected and unaffected family members from 12 kindreds. MEASUREMENTS: Anti-thyroglobulin and anti-microsomal autoantibody status was determined using an enzyme-linked immunosorbent assay. Thyrotrophin levels were determined by an immunoradiometric assay. RESULTS: Of the family members, 41.4% had evidence of autoimmune thyroid Disease, with significant co-segregation between the presence of thyroid autoantibodies and the development of Alzheimer's Disease (P less than 0.01). CONCLUSIONS: This study demonstrates a very high prevalence of autoimmune thyroid Disease in Familial Alzheimer's Disease kindreds and suggests that a genetic factor contributing towards the development of autoimmune thyroid Disease may be located on chromosome 21 within close proximity to the Familial Alzheimer's Disease gene.

Francisco Lopera - One of the best experts on this subject based on the ideXlab platform.

  • perfil clinico y cognitivo de la atrofia cortical posterior y sus diferencias con la enfermedad de alzheimer esporadica tardia y familiar precoz clinical and cognitive profile of posterior cortical atrophy and its differences with late sporadic and e
    2010
    Co-Authors: Julian Carvajal Castrillon, Daniel Camilo Aguirre, Francisco Lopera
    Abstract:

    RESUMENI ntroduccIon . La atrofia cortical posterior (ACP) es una demencia focal que se manifiesta al inicio con trastornos cognitivos posteriores, principalmente alteracion visuoperceptual por el dano en la corteza occipitoparietal, lo que permite en la clinica diferenciarla de la enfermedad de Alzheimer (EA). o bjetIvos . Analizar y comparar el rendimiento cognitivo de pacientes con ACP y con EA. M aterIales y Metodos . La muestra estuvo formada por los siguientes grupos: cuatro pacientes con ACP, siete con EA familiar precoz, nueve con EA esporadica tardia y cuatro controles sanos. A cada participante se le aplico un protocolo de evaluacion neuropsicologica para valorar procesos cognitivos y funcionalidad. La comparacion entre grupos se realizo utilizando la prueba no parametrica U de Mann-Whitney. r esultados . Los pacientes con ACP obtuvieron puntuaciones significativamente inferiores en praxias constructivas e ideacionales, lectura, calculo y visuopercepcion, respecto a ambos grupos de EA. Por el contrario, en memoria verbal, fluidez semantica y funcion ejecutiva, el grupo con ACP presento mejor desempeno.

Ghamim Ullah - One of the best experts on this subject based on the ideXlab platform.

  • impaired mitochondrial function due to Familial Alzheimers Disease causing presenilins mutants via calcium disruptions
    Cell Calcium, 2016
    Co-Authors: Patrick Toglia, Kingho Cheung, Ghamim Ullah
    Abstract:

    Abstract Mutants in presenilins (PS1 or PS2) is the major cause of Familial Alzheimer's Disease (FAD). FAD causing PS mutants affect intracellular Ca 2+ homeostasis by enhancing the gating of inositol trisphosphate (IP 3 ) receptor (IP 3 R) Ca 2+ release channel on the endoplasmic reticulum, leading to exaggerated Ca 2+ release into the cytoplasm. Using experimental IP 3 R-mediated Ca 2+ release data, in conjunction with a computational model of cell bioenergetics, we explore how the differences in mitochondrial Ca 2+ uptake in control cells and cells expressing FAD-causing PS mutants affect key variables such as ATP, reactive oxygen species (ROS), NADH, and mitochondrial Ca 2+ . We find that as a result of exaggerated cytosolic Ca 2+ in FAD-causing mutant PS-expressing cells, the rate of oxygen consumption increases dramatically and overcomes the Ca 2+ dependent enzymes that stimulate NADH production. This leads to decreased rates in proton pumping due to diminished membrane potential along with less ATP and enhanced ROS production. These results show that through Ca 2+ signaling disruption, mutant PS leads to mitochondrial dysfunction and potentially to cell death.

P Roques - One of the best experts on this subject based on the ideXlab platform.

  • association between autoimmune thyroid Disease and Familial Alzheimers Disease
    Clinical Endocrinology, 1991
    Co-Authors: Dl Ewins, Martin N Rossor, J Butler, P Roques, Michael Mullan, Alan Mcgregor
    Abstract:

    OBJECTIVE: To determine the prevalence of autoimmune thyroid Disease in Familial Alzheimer's Disease kindreds and to ascertain whether there is any evidence for genetic linkage between the two conditions. DESIGN: Retrospective study of Familial Alzheimer's Disease kindreds. PATIENTS: Seventy affected and unaffected family members from 12 kindreds. MEASUREMENTS: Anti-thyroglobulin and anti-microsomal autoantibody status was determined using an enzyme-linked immunosorbent assay. Thyrotrophin levels were determined by an immunoradiometric assay. RESULTS: Of the family members, 41.4% had evidence of autoimmune thyroid Disease, with significant co-segregation between the presence of thyroid autoantibodies and the development of Alzheimer's Disease (P less than 0.01). CONCLUSIONS: This study demonstrates a very high prevalence of autoimmune thyroid Disease in Familial Alzheimer's Disease kindreds and suggests that a genetic factor contributing towards the development of autoimmune thyroid Disease may be located on chromosome 21 within close proximity to the Familial Alzheimer's Disease gene.