Reprint

Neurodegenerative Disease: From Molecular Basis to Therapy

Edited by
February 2024
382 pages
  • ISBN978-3-7258-0188-6 (Hardback)
  • ISBN978-3-7258-0187-9 (PDF)

This book is a reprint of the Special Issue Neurodegenerative Disease: From Molecular Basis to Therapy that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

Neurodegenerative diseases are a heterogeneous, largely age-related group of disorders, characterised by the progressive degeneration or death of neurons in the central or peripheral nervous system. The prevalence of these diseases is increasing, in part due to the ageing of the population, with a consequent growing economic burden on healthcare systems. Although, in some cases, these diseases can be managed with treatments, current therapies are mostly symptomatic, do not address the underlying cause of the disease and have little or no effect on disease progression.This Special Issue aims to provide an up-to-date overview of the progress made in research into neurodegenerative diseases, from understanding the molecular basis, to establishing more effective diagnostic tools, to developing new therapies. Some papers focus on Alzheimer's disease, Parkinson's disease, motor neuron disease and Huntington's disease. Others address more general aspects of neurodegeneration, ranging from the common mechanisms of cellular damage to the role of dietary effects on the nervous system. Overall, this Special Issue highlights the continuing efforts of the scientific community to unravel the molecular basis of disease onset and progression, to achieve earlier diagnosis, to identify novel therapeutic targets and, ultimately, to develop more effective therapies to counteract the progression of these still fatal diseases.

Format
  • Hardback
License
© 2022 by the authors; CC BY-NC-ND license
Keywords
Alzheimer’s disease; toxic amyloids; Aβ; tau; genetics; amyloid clearance; vascular dysfunction; neuroinflammation; heat shock proteins; drug targets; glutathione; oxidative stress; redox signaling; glyceraldehyde-3-phosphate dehydrogenase; hydrogen peroxide; neurodegenerative disease; molecular dynamic simulation; Parkinson’s disease; deep brain stimulation; adaptive stimulation; multi-site stimulation; thalamocortical relay; basal ganglia model; local field potential; Huntington’s disease; lysosome; NAADP; two-pore channels; diabetic neuropathy; neurological damage during delivery; depression; macronutrients; mineral elements; appropriate supplementation; overdose or deficiency; Parkinson’s disease; andrographolide; MPP+; SH-SY5Y cells; ROS; Nrf2; mitophagy; protein aggregates; proteostasis; aging; age-related neurodegenerative diseases; autophagy; ubiquitin-proteasome system; ARL6IP5 (ADP-ribosylation-like factor 6 interacting protein 5); Parkinson’s disease (PD); autophagy; neurodegeneration; α-synuclein; SH-SY5Y cells; LAR; Parkinson’s disease; astrocyte; mitochondrial function; neuron; rotenone; Alzheimer’s disease; dementia; cognition; peripheral blood; algorithm; early diagnosis; experimental models of neurological diseases; vitamin E; alpha tocopherol; experimental models; Alzheimer’s disease; psychosis; dopamine; ventral hippocampus; parvalbumin; α5-GABAA; the amyloid cascade hypothesis 2.0 (ACH2.0); intraneuronal Aβ (iAβ); Aβ protein precursor (AβPP)-independent generation of iAβ; aging-related cognitive dysfunction (AACD); iAβ depletion therapy for AD and AACD; BACE1 and BACE2 activators as AD and AACD drugs; brain transcriptome; migratory birds; spring migration; wintering; Calidris pusilla; PKCε; PRKCE; amyotrophic lateral sclerosis; neurodegeneration; Bryostatin-1; methamphetamine; neurodegeneration; substantia nigra pars compacta; locus coeruleus; monoamine oxidase; sex difference; α7 nicotinic acetylcholine receptor; TLR4; TLR2; CXCR4; CD4; CCR5; TR-FRET; neurodegenerative disease; Alzheimer’s disease; amyloid precursor protein (APP); amyloid beta; protein biogenesis; protein transport; membrane proteins; SRP-dependent targeting; n/a