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Journal of Neurology and Neurorehabilitation Research | Volume: 3
August 16-17, 2018 | Copenhagen, Denmark
Dementia and Alzheimer ’s Disease
10
th
World congress on
N
europlasticity is both a substrate of learning and memory
and a mediator of responses to neuronal cell attrition
and injury. It is a continuous process in reaction to neuronal
activity and injury, death, and genesis, involving modulation
of structural/functional processes of axons, dendrites, and
synapses. Structural elements that embody plasticity include
long-term potentiation (a cellular correlate of learning
and memory), synaptic efficacy, synaptic remodeling,
synaptogenesis, neurite extension including axonal sprouting
and dendritic remodeling, and neurogenesis and recruitment.
As research on human neurodegeneration has moved from
descriptive phenomenology to mechanistic analysis, it has
become increasing apparent that the morphological lesions
long used by neuropathologists to confirm a clinical diagnosis
after death might provide an experimentally tractable handle
to understand causative pathways. For example, Alzheimer
disease (AD) is an aging-dependent neurodegenerative
disorder characterized neuropathologically by deposition
of insoluble amyloid β-peptide (Aβ) in extracellular plaques
and aggregated tau protein, which is found largely in the
intracellular neurofibrillary tangles. We now appreciate
that mild cognitive impairment in early AD may be due to
synaptic dysfunction caused by accumulation of non-fibrillar,
oligomeric Aβ, well before widespread synaptic loss and
neurodegeneration become evident. Soluble Aβ oligomers can
adversely affect synaptic structure and plasticity at extremely
lowconcentrations, although themolecular substrates bywhich
synaptic memory mechanisms are disrupted remain to be fully
elucidated. A primary locus of excitatory synaptic transmission
in themammalian central nervous system is the dendritic spine.
Loss of spine density has been linked to cognitive and memory
impairment in AD. We will review current knowledge on the
bases of synaptic dysfunction in neurodegenerative diseases,
with a focus on AD, and will cover both amyloid- and non-
amyloid-driven mechanisms. Consideration will also be given to
emerging data which point to potential therapeutic approaches
for ameliorating the cognitive and memory deficits associated
with these disorders.
Speaker Biography
Stephen Skaper received a PhD in biochemistry from the University of South Dakota
and Laurea in chemistry from the University of Padua, Italy. He is currently Adjunct
Professor in the Department of Pharmaceutical and Pharmacological Sciences (section
on Pharmacology and Anesthesiology) at the University of Padua. Previously he was a
Senior Group Leader for Neurodegeneration Research, Neurology Centre of Excellence
for Drug Discovery, GlaxoSmithKline Research and Development Limited, United
Kingdom, and also held academic research positions in the Departments of Medicine
and Biology at the University of California, San Diego. Skaper has authored/co-authored
over 300 research papers, as well as having guest-edited journal thematic issues and
two volumes of Methods in Molecular Biology on neurotrophic factors. He is Editor-in-
Chief of CNS & Neurological Disorders Drug Targets, a Councilor of the International
Association of Neurorestoratology, and a member of Sigma ΧI, Phi Lambda Upsilon,
and the Society for Neuroscience.
e:
stephen.skaper@unipd.itStephen Skaper
University of Padua, Italy
Synaptic plasticity, Dementia and Alzheimer’s Disease