Differences in
synaptic dysfunction between rTg4510 and APP / PS1 mouse models of Alzheimer's disease S GELMAN, J PALMA, P KABITZKE, G TOMBAUGH, A GHAVAMI... Abstract / Posters
Our purpose is to better understand synapthopathies in general with a special focus
on synaptic dysfunction induced by autoantibodies.
Cellular and molecular basis
of synaptic dysfunction and aberrant behavior in autism, tuberous sclerosis complex, and Angelman syndrome
Santini, E., Turner, K.L., Ramaraj, A.B., Klann, E. *, and Kaphzan, H. * (2015) Mitochondrial superoxide contributes to
hippocampal synaptic dysfunction and memory deficits in Angelman syndrome model mice.
In an earlier study published in Nature Medicine, an international team of scientists discovered that the additional copy of chromosome 21 in Down's syndrome reduces the production of SNX27 in the brain and results
in synaptic dysfunction.
The protein's role in the pathway leading to memory impairment, however, remained unclear until scientists from IMCB utilised live - cell imaging techniques to elucidate the mechanism of memory impairment and illustrated how SNX27 attributes to
synaptic dysfunction.
The study implicitly suggests that dementia is associated with
a synaptic dysfunction rather than the disappearance of synapses from the patient's cortex.
Like humans with AD, hAPP mice have elevated levels of amyloid β (Aβ) peptides in the brain, network and
synaptic dysfunction, and amyloid plaques (9).
reports underline that tau may be localized within both pre - and post-synaptic compartments, suggesting that it may possibly induce or contribute to
synaptic dysfunction.
Recent... reports underline that tau may be localized within both pre - and post-synaptic compartments, suggesting that it may possibly induce or contribute to
synaptic dysfunction.
In principle, these homeostatic mechanisms could be harnessed to counteract cognitive decline and
synaptic dysfunction in aging nervous systems.
Alzheimer's disease (AD) is characterized by deposition of amyloid - β (Aβ) plaques and neurofibrillary tangles in the brain, accompanied by
synaptic dysfunction and neurodegeneration.
Host: Dr. Miriam Spering Speaker: Dr. Lynn Raymond, UBC Title:
Synaptic dysfunction in prodromal Huntington disease
Additionally,
synaptic dysfunction is evident in early development of pathology.
Notably, we have found that prolonged activation of these pathways results in altered translational control, which contributes to
synaptic dysfunction and memory deficits in AD model mice.
One food may be able to combat all four purported causal factors of autism:
synaptic dysfunction, oxidative stress, mitochondrial dysfunction, and neuroinflammation.
Creates massive changes to their structure, including cell death and
synaptic dysfunction.