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The pace of life for forest trees

9 months ago
Science, Volume 386, Issue 6717, Page 92-98, October 2024.
Lalasia Bialic-Murphy, Robert M. McElderry, Adriane Esquivel-Muelbert, Johan van den Hoogen, Pieter A. Zuidema, Oliver L. Phillips, Edmar Almeida de Oliveira, Patricia Alvarez Loayza, Esteban Alvarez-Davila, Luciana F. Alves, Vinícius Andrade Maia,…

Creation of de novo cryptic splicing for ALS and FTD precision medicine

9 months ago
Science, Volume 386, Issue 6717, Page 61-69, October 2024.
Oscar G. Wilkins, Max Z. Y. J. Chien, Josette J. Wlaschin, Simone Barattucci, Peter Harley, Francesca Mattedi, Puja R. Mehta, Maria Pisliakova, Eugeni Ryadnov, Matthew J. Keuss, David Thompson, Holly Digby, Lea Knez, Rebecca L. Simkin, Juan Antinao Diaz,…

Bridging brain insulin resistance to Alzheimer's pathogenesis

9 months ago
Emerging evidence links type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD), with brain insulin resistance (BIR) as a key factor. In a recent study, Lanzillotta et al. reveal that reduced biliverdin reductase-A (BVR-A) impairs glycogen synthase kinase 3β (GSK3β) phosphorylation, causing mitochondrial dysfunction and exacerbating brain insulin resistance in the progression of both T2DM and AD.
Wenqiang Chen

The role of PINK1-Parkin in mitochondrial quality control

9 months ago
Mitophagy mediated by the recessive Parkinson's disease genes PINK1 and Parkin responds to mitochondrial damage to preserve mitochondrial function. In the pathway, PINK1 is the damage sensor, probing the integrity of the mitochondrial import pathway, and activating Parkin when import is blocked. Parkin is the effector, selectively marking damaged mitochondria with ubiquitin for mitophagy and other quality-control processes. This selective mitochondrial quality-control pathway may be especially...
Derek P Narendra

Midlife dynamics of white matter architecture in lexical production

9 months ago
We aimed to examine the white matter changes associated with lexical production difficulties, beginning in midlife with increased naming latencies. To delay lexical production decline, middle-aged adults may rely on domain-general and language-specific compensatory mechanisms proposed by the LARA model (Lexical Access and Retrieval in Aging). However, the white matter changes supporting these mechanisms remains largely unknown. Using data from the CAMCAN cohort, we employed an unsupervised and...
Clément Guichet