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Science, Ahead of Print.

The Alzheimer’s risk gene APOE4 may actively damage brain blood vessels and sabotage the cellular systems that remove harmful proteins. Researchers were able to reverse some of these effects in experiments, revealing promising new targets for Alzheimer’s, Parkinson’s, and other neurodegenerative diseases.

Experimental reactor needed much more uranium and heavy water than the country could muster

A common mistake during blood pressure checks could make readings appear substantially higher than they really are. Johns Hopkins researchers found that leaving the arm unsupported can raise systolic readings by about 6.5 mmHg, potentially affecting a hypertension diagnosis.

Shifts in blood proteins could point to ways to fight menopause “brain fog” and prevent later dementia

Companies striving to reduce continent’s reliance on foreign shots must overcome major financial and logistical challenges

A review of more than 265,000 people found that cannabis use was associated with higher rates of both committing violence and becoming a victim of it. The researchers say the link is significant but does not prove cannabis itself is the cause.

Mulberry compounds may reshape the gut microbiome in ways that support intestinal health and metabolism, with some combinations showing especially strong effects in animal studies. However, the results vary depending on the plant part and processing method, and the benefits have yet to be confirmed in humans.

Optical illusions trick enemies into misjudging the insects’ speed and direction

Google DeepMind team inserts identifiable pattern into protein’s sequence without compromising its structure or function

In Alzheimer's Disease (AD) the default mode network (DMN) exhibits selective vulnerability to functional decline and amyloid beta (Aβ) plaques in early AD. DMN vulnerability may simply be the result of Aβ accumulation. Alternately, Aβ may unmask an intrinsic susceptibility of DMN circuits. Should DMN vulnerability persist amidst global Aβ deposition, this would support the latter hypothesis. We tested this using long-term, multi-region recordings of single units in mice characterized by...

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Alternative polyadenylation (APA) has a central role in regulation of the fate of mRNA and exhibits high variability in the brain and in neurons. However, brain APA regulation has not been mapped at cell type resolution, and the genetic control of APA in brain cell types and its contribution to genetic disease have remained unclear. Here we report a single-cell atlas of APA of the aged human brain across 2 million cells from 379 human postmortem brains across individuals with and without...

Most neurodegenerative diseases are thought to spread through the brain by prion-like mechanisms, in which filamentous protein assemblies self-propagate by templated seeding¹. Distinct conformations of amyloid filaments may provide the physical basis for the strains that lead to different diseases². However, a central pillar of the prion hypothesis, that strains retain their structural identity upon transmission, has not been demonstrated. Here we show that the injection of tau filaments from...

Hutchinson Gilford progeria syndrome (HGPS) is a fatal premature aging disorder caused by pathogenic farnesylated lamin A variants that disrupt nuclear architecture and DNA repair. Current therapies, including farnesyltransferase inhibitors, provide only modest survival benefits and lack molecular specificity, while mutation-specific genome-editing strategies cannot address atypical laminopathies. Here, we develop Farnesylation Amino acid Targeted Editing (FATE), a mutation-agnostic base-editing...

Estrogen Receptor alpha (ERα) is the primary driver in ER+ breast cancer and can be targeted using small molecules such as fulvestrant, a selective estrogen receptor degrader (SERD). Despite being approved over two decades ago and used regularly in post-menopausal women, its precise anti-tumor mechanism remains unclear, with several reports showing efficacy without the requirement for ERα degradation. To investigate the molecular basis of fulvestrant's action, we employed split intein-based µMap...

Ageing has been described through many theoretical frameworks, yet its mechanistic basis remains unresolved. Here we propose that ageing reflects progressive decanalization of mammalian cell identity, driven by erosion of a regulatory grammar written during development. Extending Waddington's epigenetic landscape, development canalizes cell fates through globally coordinated chromatin programs that establish identity constraints across multiple timescales. Subsequently, these constraints can...

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