<p>APLNR expression is upregulated in the infiltrating tumor zone in glioblastoma.</p>

Apelin expression is correlated with angiogenesis in human glioblastoma.

Apelin expression is correlated with angiogenesis in human glioblastoma.

<p>APLNR expression is upregulated in the infiltrating tumor zone in glioblastoma.</p>

<p>Glioblastoma cell- and host-derived apelin controls tumor angiogenesis.</p>

APLNR is expressed in glioblastoma cells and receptor internalization is activated by apelin peptides specifically.

<p>Apelin is expressed in tumor vessels.</p>

Supplementary Text and Methods

APLNR expression is upregulated in the infiltrating tumor zone in glioblastoma.

Apelin is expressed in tumor vessels.

<p>Apelin is expressed in tumor vessels.</p>

Apelin is expressed in tumor vessels.

<p>Anti-invasive role of apelin in orthotopic models of proneural and classical glioblastoma.</p>

APLNR is expressed in glioblastoma cells and receptor internalization is activated by apelin peptides specifically.

Anti-invasive role of apelin in orthotopic models of proneural and classical glioblastoma.

Supplementary Text and Methods

APLNR expression is upregulated in the infiltrating tumor zone in glioblastoma.

APLN co-expressed genes are enriched for angiogenesis in glioblastoma subtypes

<p>Anti-invasive role of apelin in orthotopic models of proneural and classical glioblastoma.</p>

During aging, lifestyle-related factors shape the brain's response to insults and modulate the progression of neurodegenerative pathologies such as Alzheimer's disease (AD). This is the case for chronic hyperglycemia associated with type 2 diabetes, which reduces the brain's ability to handle the neurodegenerative burden associated with AD. However, the mechanisms behind the effects of chronic hyperglycemia in the context of AD are not fully understood. Here, we show that newly generated neurons in the hippocampal dentate gyrus of triple transgenic AD (3xTg-AD) mice present increased dendritic arborization and a number of synaptic puncta, which may constitute a compensatory mechanism allowing the animals to cope with a lower neurogenesis rate. Contrariwise, chronic hyperglycemia decreases the complexity and differentiation of 3xTg-AD newborn neurons and reduces the levels of β-catenin, a key intrinsic modulator of neuronal maturation. Moreover, synaptic facilitation is depressed in hyperglycemic 3xTg-AD mice, accompanying the defective hippocampal-dependent memory. Our data suggest that hyperglycemia evokes cellular and functional alterations that accelerate the onset of AD-related symptoms, namely memory impairment.