Tufts researchers have developed neurotransmitter-lipid hybrids that help transport therapeutic drugs and gene editing proteins across the blood-brain barrier in mice.
APOE4, a gene implicated as a risk factor for Alzheimer's disease, triggers leaks in the blood-brain barrier. The damage to capillaries APOE4 causes correlates with increased levels of cyclophilin, a protein that causes the inflammation that is a signature of early Alzheimer's.
Researchers have developed a cyclic peptide that can enhance blood-brain barrier penetration.
Microglia initially protects the blood-brain barrier from damage due to systemic inflammation. However, microglia can alter their behavior and increase the permeability of the blood-brain barrier, thus damaging it.
Older mice given anti-inflammatory medication were better able to learn new tasks and became almost as adept at learning as mice half their age.
A synthesized small-molecule drug blocks the TGF-beta receptor in astrocytes and traverses the blood-brain barrier in mice. When administered, the drug lowered receptor activity to that seen in younger mice and reduced inflammation. The aged mice were able to navigate mazes and learn spatial tasks as well as younger mice.
Using transcranial focused ultrasound in combination with injectable microbubbles, researchers open a pathway through the blood-brain barrier. The technique allows drugs to penetrate the brain and trigger therapeutic effects for those with neurodegenerative diseases.
Using induced pluripotent stem cells derived from patients with neurodegenerative disorders, researcher recreated the blood-brain barrier inside Organ-Chips.
Cannabidiol may be able to bypass the blood-brain barrier to effectively deliver medications directly to the brain.
A new study reports damage to the blood-brain barrier can cause age related cognitive decline, and sheds light on how we could reverse the aging process in the brain.
A new study reports leaky capillaries in the brain may be an early sign of Alzheimer's disease as it can signal cognitive impairment prior to the buildup of proteins associated with the neurodegenerative disease.