Alzheimer’s disease pathology reversed in mouse model
Researchers have observed improvements in the cognitive function of mice after reversing the formation of beta-amyloid plaques.
Researchers have observed improvements in the cognitive function of mice after reversing the formation of beta-amyloid plaques.
A new study implicates a novel gene target in the efficacy of electroconvulsive therapy as a depression treatment.
Researchers have discovered that an experimental drug appears to block the flow of toxic ions thought to cause Alzheimer’s.
For the first time, researchers have been able to examine the exact link between amyloid- β and tau in an animal model of the Alzheimer’s brain, providing hope for new therapeutic targets.
An international consortium has used mouse knockouts to identify 52 novel genes associated with hearing.
Neural activity resembling epileptic events has been found in multiple GCaMP6-expressing transgenic mouse lines, potentially complicating interpretation of neural activity in the lines.
Research suggests increasing synaptic activity could alleviate SMA symptoms: motor function of mice was improved when treated with a glutamate receptor stimulant.
Reducing mouse model brain levels of the protein Ephexin5 prevented the loss of excitatory synapses that typically leads to memory loss in Alzheimer’s disease.
Researchers at Colombia University, New York (NY, USA), have recently demonstrated that tau pathology induces dysfunction in cells specifically tuned to compute spatial information.
In this interview, Drs Silverman and Buscher discuss their work, and how these two rare diseases are shedding light not only on each other, but also a wealth of other neurological disorders.