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
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.
Not exact matches
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.
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).
In principle, these homeostatic mechanisms could be harnessed to counteract cognitive decline and synaptic dysfunction in aging nervous system
In principle, these homeostatic mechanisms could be harnessed to counteract cognitive decline and
synaptic dysfunction in aging nervous system
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.
Our purpose is to better understand synapthopathies
in general with a special focus on
synaptic dysfunction induced by autoantibodies.
The goal of our research is to better understand the cellular and molecular mechanisms involved
in neuronal and
synaptic dysfunctions characterizing neuropsychiatric diseases.
Published on April 20
in the journal Molecular Psychiatry, this work reveals that the loss of function of this gene involved
in intellectual disability and autism, leads to
synaptic dysfunction.
Host: Dr. Miriam Spering Speaker: Dr. Lynn Raymond, UBC Title:
Synaptic dysfunction in prodromal Huntington disease
Francesco Longo is interested
in understanding the
synaptic and behavioral abnormalities associated with autism spectrum disorder, with particular attention to striatal
dysfunction in fragile X syndrome model mice.
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.
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.
Enhanced amyloidogenic processing of APP by the ß - site APP cleaving enzyme (BACE) and the γ - secretase complex and reduced clearance lead to increased intracellular levels of soluble oligomeric Aß, resulting
in cellular
dysfunction comprising e.g.,
synaptic failure, mitochondrial
dysfunction, enhanced oxidative stress, neurotransmitter and neurotrophin depletion, inflammation, and apoptosis which is reflected
in patients as clinical symptoms such as cognitive deficits [2, 3].
We believe that this 10 - lipid phospholipid biomarker panel reflects the breakdown of neural cell membranes
in those individuals destined to develop advanced moderate cognitive impairment or Alzheimer's disease and may mark the transition between preclinical states where
synaptic dysfunction and early neurodegeneration give rise to subtle cognitive changes.»