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Microbial BMAA elicits mitochondrial dysfunction, innate immunity activation, a...

Silva, Diana F.; Candeias, Emanuel; Esteves, Ana Raquel Fernandes; Magalhães, João Duarte; Ferreira, I. Luísa; Nunes-Costa, Daniela; Rego, Ana Cristina

Background: After decades of research recognizing it as a complex multifactorial disorder, sporadic Alzheimer’s disease (sAD) still has no known etiology. Adding to the myriad of different pathways involved, bacterial neurotoxins are assuming greater importance in the etiology and/or progression of sAD. β-N-Methylamino-L-alanine (BMAA), a neurotoxin produced by some microorganisms namely cyanobacteria, was prev...


Activation of IGF-1 and Insulin Signaling Pathways Ameliorate Mitochondrial Fun...

Naia, Luana; Ferreira, I. Luísa; Cunha-Oliveira, Teresa; Duarte, Ana I.; Ribeiro, Márcio; Rosenstock, Tatiana R.; Laço, Mário N.; Ribeiro, Maria J.

Huntington's disease (HD) is an inherited neurodegenerative disease caused by a polyglutamine repeat expansion in the huntingtin protein. Mitochondrial dysfunction associated with energy failure plays an important role in this untreated pathology. In the present work, we used lymphoblasts obtained from HD patients or unaffected parentally related individuals to study the protective role of insulin-like growth f...


Bioenergetic dysfunction in Huntington's disease human cybrids

Ferreira, I. Luísa; Cunha-Oliveira, Teresa; Nascimento, Maria V.; Ribeiro, Márcio; Proença, M. Teresa; Januário, Cristina; Oliveira, Catarina R.

In this work we studied the mitochondrial-associated metabolic pathways in Huntington's disease (HD) versus control (CTR) cybrids, a cell model in which the contribution of mitochondrial defects from patients is isolated. HD cybrids exhibited an interesting increase in ATP levels, when compared to CTR cybrids. Concomitantly, we observed increased glycolytic rate in HD cybrids, as revealed by increased lactate/p...


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