This special topic issue of 'Neurodegenerative Diseases' contains contributions discussing the subject in-depth. 'Neurodegenerative Diseases' is a well-respected, international peer-reviewed journal in 'Neurobiology'. Special topic issues are included in the subscription.

Alzheimer’s Disease (AD) is the product of the slow and progressive degenerative alteration that develops in the adult brain and can remain asymptomatic for a considerable time before cognitive deficits becomes evident. The main challenge for researchers is to identify markers of this degenerative process, and, in this sense, data has been generated through experiments bringing to light new mechanisms and hypothesis to explain its pathophysiology. This book is a review of recent studies in AD molecular biology. Chapters explain various facets of AD, which include animal models, morphological changes, membrane composition, amyloidogenic peptides, intracellular transport systems, and the role of oxidative stress and calcium deregulation. Readers will understand the molecular mechanisms behind AD and therefore broaden their perspective on this neurodegenerative disease and its progression.

A biochemical hypothesis - that Alzheimer’s disease (AD) is a progressive cerebral amyloidosis caused by the aggregation of the amyloid b-protein (Ab) - preceded and enabled the discovery of etiologies. This volume serves as a record focused on bringing together investigators at the forefront of elucidating the structure and function of hippocampal synapses with investigators focused on understanding how early assemblies of Ab may compromise some of these synapses.

Alzheimer’s disease (AD) is an age-related neurological disease that affects tens of millions of people, in addition to their carers. Hallmark features of AD include plaques composed of amyloid beta, as well as neurofibrillary tangles of tau protein. However, despite more than a century of study, the cause of Alzheimer’s disease remains unresolved. The roles of amyloid beta and tau are being questioned and other causes of AD are now under consideration. The contributions of researchers, model organisms, and various hypotheses will be examined in this Special Issue.

Synapses are complex, highly specialized biological structures. Therefore, even slight functional disturbance can lead to disruptive brain disorders. Dysfunction of these structures is associated with a variety of aging-related neurodegenerative conditions, such as Alzheimer's and Parkinson's disease. Most synaptopathies compromise complex signaling pathways by progressively affecting the synaptic protein repertoire. Currently, the treatment of most of these pathologies focuses on the mitigation of symptoms; in consequence, further efforts need to be made to elucidate the common molecular culprit and cellular mechanisms underlying the cause of these severe pathologies to serve as therapeutic targets for clinical applications. In this Research Topic, we aim to discuss synaptic dysfunction as a causal factor for aging-related neurodegenerative diseases. Despite the recent technological advances that allow identifying the individual synaptic components affected in these synaptic pathologies, we know little about how they impact the synaptic function. To promote the discussion around the molecular and functional connection, we primarily welcome original research, review, and perspective articles emphasizing the relationship between synaptic function and the proteins or mechanisms affected.

This volume is a companion to the highly successful book published in association with the Journal of Alzheimer's Disease (JAD) on the centennial of Alzheimer's discovery: "Alzheimer's Disease: A Century of Scientific and Clinical Research". Instead of looking back, this collection, "Alzheimer's Disease: Advances for a New Century", will look forward. Using scientometric analysis the most promising developments since the Alzheimer Centennial in 2006 have been substantiated. While prior trends and advances in genetics, amyloid-β, tau, neuropathology, and oxidative stress continue as active areas, emergent areas impacting the transition from normal cognition to Alzheimer's disease such as diagnostic imaging, biomarkers, metabolism, and lifestyle (areas conceived only a few years ago) now dominate the debate.Invited contributors have summarized their landmark publications identified by our analysis and have put them into perspective, explaining the impetus behind the work, the contribution of the results to the field, and who played a role in the work.