Lipids in Neurodegenerative Diseases

Dear Colleagues,

Proteopathy (protein disease) is a term coined by Walker and LeVine (Neurobiology of Aging 21, 559–561, 2000) to define disparate diseases of the nervous system, characterized by malfunctioning endogenous protein monomers becoming conformationally unstable, prone to self-polymerize in small and large aggregates, known as oligomers and fibrils, producing neuronal damage. Each specific protein, in acquiring a strong tendency to self-aggregate, regardless of its physiological function, can underline a specific neurodegenerative process. Some of the most common neurodegenerative proteopathies are Alzheimer’s disease (AD), Parkinson’s disease (PD), Creutzfeldt–Jacob disease (CJD), dementia with Lewy bodies (DLB), Huntington disease (HD), and amyotrophic lateral sclerosis (ALS).

In recent decades, compelling evidence has demonstrated that oligomers are toxic and per se sufficient to induce a pathological cascade involving the cell membrane, mitochondrial damage, and reactive inflammation, finally leading to degeneration of the central nervous system; by contrast, fibrillar large aggregates may be relatively benign.

Many efforts have been made to understand factors leading to proteins’ conformational changes. In some instances, proteins’ instability and increased tendency to polymerize are due to point mutations in the encoding genes, which are responsible for the familial hereditary forms of neurodegenerative diseases. However, the most prevalent cases of typical proteopathies are of unknown origin. In recent years, a lot of studies have focused on lipids, constituting globally about 50% of brain tissue, and on the multidimensional roles that they may have in the pathogenic processes of common neurodegenerative diseases.

It has been shown that lipids can interact particularly with the aggregation and propagation of pathogenic proteins, e.g., amyloid-β, tau, and α-synuclein, underlying the neurodegenerative processes of AD, FTD, PD, and DLB. Moreover, lipids can influence other key aspects of neurodegenerative disease pathophysiology, which are mitochondrial dysfunction, inflammation, and oxidative stress.

This Special Issue on “Lipids in Neurodegenerative Diseases” aims to collect original research and review articles on the multifaceted role that lipids may have on differentiated pathophysiological cascades, leading to the most common as well as to less common neurodegenerative proteopathies.

Prof. Dr. Giuseppe Sancesario
Dr. Valerio Chiurchiù
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.