The etiology of early onset Alzheimer's disease (AD) is genetic in nature for the vast majority of patients, with the mutations involved primarily located in pathways dealing with processing of β-amyloid peptide. However, much research over the last two decades has established that, while one or more genetic risk factors have been identified for development of late-onset AD, that disease is not primarily genetic in origin. Research in the field has been strongly influenced by the Amyloid Cascade Hypothesis, which posits that plaques of β-amyloid (neuritic senile plaques, NSP) accumulate in the neuropil, subsequently initiating a neuropathogenic process that engenders insoluble tangles of modified tau protein (neurofibrillary tangles, NFT), and ultimately to progressive cognitive dysfunction. Firm diagnosis of the disease still depends primarily on postmortem examination of the density and character of NSP and NFT in the affected brain. Inflammation in the AD brain has been documented but has not found a major place in the suite of factors playing primary roles in the neuropathogenesis.

Accumulating evidence from animal models and various clinical trials indicates that late-onset AD is not adequately explained solely or primarily by NSP and NFT, even though these are the most obvious and consistent pathological features of this disease. Rather, late-onset AD appears to result from a complex interplay between genetic and environmental factors, both aspects of which remain to be elucidated. We are interested in submissions that present alternate viewpoints regarding the apparently complex etiology and pathogenic processes underlying late-onset AD. Articles in the form of primary research papers, reviews of recent developments focusing on etiology and neuropathogenic mechanisms in AD, or hypothesis-driven but evidence-based arguments all will be appropriate. Potential topics include, but are not limited to:

• Information from comparative genome sequencing studies that shed new light on the complex genetic background providing increased susceptibility to disease induction
• Information concerning possible environmental influences for induction of late-onset AD
• Recent insights related to the origin and role of inflammation in the neuropathogenesis of late-onset AD
• New research into the biochemistry and molecular genetics of the AD brain
• Ideas concerning the role of the ε4 gene product from the APOE locus in conferring susceptibility to late-onset AD

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