A Critical Proton MR Spectroscopy Marker of Alzheimer's Disease Early Neurodegenerative Change: Low Hippocampal NAA/Cr Ratio Impacts APOE ɛ4 Mexico City Children and Their Parents.

Severe air pollution exposures produce systemic, respiratory, myocardial, and brain inflammation and Alzheimer's disease (AD) hallmarks in clinically healthy children. We tested whether hippocampal metabolite ratios are associated with contrasting levels of air pollution, APOE, and body mass index (BMI) in paired healthy children and one parent sharing the same APOE alleles. We used 1H-MRS to interrogate bilateral hippocampal single-voxel in 57 children (12.45 ± 3.4 years) and their 48 parents (37.5 ± 6.78 years) from a low pollution city versus Mexico City (MC). NAA/Cr, Cho/Cr, and mI/Cr metabolite ratios were analyzed. The right hippocampus NAA/Cr ratio was significantly different between cohorts (p = 0.007). The NAA/Cr ratio in right hippocampus in controls versus APOE ɛ4 MC children and in left hippocampus in MC APOE ɛ4 parents versus their children was significantly different after adjusting for age, gender, and BMI (p = 0.027 and 0.01, respectively). The NAA/Cr ratio is considered reflective of neuronal density/functional integrity/loss of synapses/higher pTau burden, thus a significant decrease in hippocampal NAA/Cr ratios may constitute a spectral marker of early neurodegeneration in young urbanites. Decreases in NAA/Cr correlate well with cognitive function, behavioral symptoms, and dementia severity; thus, since the progression of AD starts decades before clinical diagnosis, our findings support the hypothesis that under chronic exposures to fine particulate matter and ozone above the standards, neurodegenerative processes start in childhood and APOE ɛ4 carriers are at higher risk. Gene and environmental factors are critical in the development of AD and the identification and neuroprotection of young urbanites at high risk must become a public health priority.

Mexico City normal weight children exposed to high concentrations of ambient PM2.5 show high blood leptin and endothelin-1, vitamin D deficiency, and food reward hormone dysregulation versus low pollution controls. Relevance for obesity and Alzheimer disease.

Millions of Mexico, US and across the world children are overweight and obese. Exposure to fossil-fuel combustion sources increases the risk for obesity and diabetes, while long-term exposure to fine particulate matter (PM2.5) and ozone (O3) above US EPA standards is associated with increased risk of Alzheimer's disease (AD). Mexico City Metropolitan Area children are chronically exposed to PM2.5 and O3 concentrations above the standards and exhibit systemic, brain and intrathecal inflammation, cognitive deficits, and Alzheimer disease neuropathology. We investigated adipokines, food reward hormones, endothelial dysfunction, vitamin D and apolipoprotein E (APOE) relationships in 80 healthy, normal weight 11.1±3.2 year olds matched by age, gender, BMI and SES, low (n: 26) versus high (n:54) PM2.5 exposures. Mexico City children had higher leptin and endothelin-1 (p<0.01 and p<0.000), and decreases in glucagon-like peptide-1 (GLP 1), ghrelin, and glucagon (<0.02) versus controls. BMI and leptin relationships were significantly different in low versus high PM2.5 exposed children. Mexico City APOE 4 versus 3 children had higher glucose (p=0.009). Serum 25-hydroxyvitamin D<30 ng/mL was documented in 87% of Mexico City children. Leptin is strongly positively associated to PM 2.5 cumulative exposures. Residing in a high PM2.5 and O3 environment is associated with 12h fasting hyperleptinemia, altered appetite-regulating peptides, vitamin D deficiency, and increases in ET-1 in clinically healthy children. These changes could signal the future trajectory of urban children towards the development of insulin resistance, obesity, type II diabetes, premature cardiovascular disease, addiction-like behavior, cognitive impairment and Alzheimer's disease. Increased efforts should be made to decrease pediatric PM2.5 exposures, to deliver health interventions prior to the development of obesity and to identify and mitigate environmental factors influencing obesity and Alzheimer disease.

Utilidad clínica de la diferencia arteriovenosa de oxígeno de las malformaciones arteriovenosas cerebrales / Clinical utility of the diference of levels of arteriovenous oxygenation in cerebral arteriovenous malformations

Se analizaron en el Hospital central sur de alta especialidad PEMEX 30 casos de pacientes con malformaciones arteriovenosas cerebrales ingresados al servicio de neurocirugía entre enero de 1995 y enero de 1999, de los cuales fueron sometidos a diferentes modalidades terapéuticas veintitrés pacientes se les realizó exéresis microquirùrgica (76.67 por ciento), 4 a radiocirugía (13.33 por ciento) y 3 a embolización (10 por ciento). Se buscó la utilidad de la obtención de un gradiente diferencial en la oxigenación venosa obtenida por la correlación entre la sangre venosa a nivel del bulbo de la vena yugular interna, comparándola con el nivel de oxigenación de la sangre arterial a nivel de la arteria radial. Dichas mediciones se realizaron en forma tanto preoperatoria como en el postoperatorio inmediato y fueron analizados los datos mediante la utilización de una fórmula para obtener un valor constante que nos permite establecer un parámetro comparativo sobre la diferencia arteriovenosa de la oxigenación normal y anormal. Pudiendo así dar un valor a la presencia de un corto circuito presente en todos los pacientes con MAV's. Se concluye que la diferencia arteriovenosa de oxigeno cerebral es un procedimiento efectivo para determinar la presencia de una malformación de manera preoperatoria y valorar el grado de efectividad del tratamiento en el postoperatorio.

Experiencia en el tratamiento de hemorragia subaracnoidea secundaria a ruptura de aneurisma intracraneal en el Centro Médico del Noreste / Experience in the treatment of subarachnoideal hemorrhage followin rupture of an intracranial aneurism at the Centro Medico del Noreste

Se ralizó un estudio a 65 pacientes con diagnóstico de hemorragia subaracnoidea (HSA) secundaria a ruptura de aneurisma cerebral de 1§ de febrero de 1991 al 31 de agosto de 1992, siguiendo por sies meses a 55 pacientes, 35 mujeres y 20 hombres. Por escala de Hunt y Hess (HH) para HSA, se situó a 23 en grado I, ocho en grado II, 19 en grado III y cinco en grado IV, por angiografía cerebral se demostró vasoespasmo en 14 y por tomografía computarizada cerebral se corroboró resangrado en diez. El intervalo entre la sintomatología la cirugía fue de seis a 136 días, promediando 21. Obteniendo en 34 pacientes buena recuperación, 12 deshabilitados y nueve defunciones. Se concluye que el diagnóstico y manejo tempranos disminuyen la morbimortalidad; aumentando ésta en los días cuatro a 13 después del sangrado, en los grados III y IV de HH, ante resangrado y vasoespasmo

Hemorragia subaracnoidea secundaria a ruptura de aneurisma intracraneal / Subarachnoid haemohrrage secondary to intracranial aneurysm rupture

La hemorragia subaracnoidea representa una importante causa de mortalidad en los servicios de neurología. El cuadro clínico es característico de comienzo brusco, y está relacionado con el esfuerzo. La punción lumbar confirma el diagnóstico y la angiografia confirma la lesión. Los pacientes en condiciones favorables deben intervenirse quirúrgicamente. Se presenta la experiencia de 1983 en el Servicio de Neurocirugía del Hospital General del Centro Médico Nacional. Se operaron 22 pacientes con mortalidad de 10 por ciento y recuperación funcional buena en 60 por ciento de los casos