Oligomeric Amyloid-β and Tau, two proteins involved in Alzheimer's disease pathogenesis, require Amyloid Precursor Protein to enter neurons and exert their detrimental effect on synaptic plasticity and memory.
M2 cortex-dorsolateral striatum circuit is functionally altered in Huntington's disease and, by boosting its activity, we reverse symptoms at behavioral, physiological, and morphological level in symptomatic mice.
The retinotectal map in zebrafish exhibits location-specific, functional specializations to match prey object movement in the visual field during the hunting sequence.
Genetic and biochemical analysis reveal a variant in HSF2BP causing POI and C19ORF57/BRME1 as an interactor and stabilizer of HSF2BP by forming a complex with BRCA2, RAD51, RPA and PALB2.
An extracellular modulator of IGF1 signaling, Pappaa, regulates endoplasmic reticulum–mitochondria connections, which are critical for metabolic homeostasis and hair cell survival.
During times of mitochondrial impairment, non-imported mitochondrial precursor proteins are targeted to the nucleus for proteasome-dependent degradation.
Iron derived from autophagy-mediated ferritin degradation in response to pressure overload induces lipid peroxidation, necrotic cardiomyocyte death, and heart failure in mice.
Morphologic, molecular, biomechanical and computational analyses show that the specialized extracellular matrix architecture of the umbilical artery contributes to its rapid closure at birth and regulates smooth muscle cell differentiation.
The midbrain area for salience, reward and aversion in mouse brain harbours among the dopamine cells three subtypes somatostatin-expressing neurons that show combinatorial neurotransmitter phenotypes and interneuron properties.
