More than 100 years after description of Alzheimer's disease (AD), two major pathological processes observed already by Alois Alzheimer, remain as the main explanation of the pathogenesis of Alzheimer's disease. Important molecular interactions leading to AD neuropathology were described in amyloid cascade and in tau protein function. No clinical trials with novel therapies based on amyloid cascade and tau protein hypotheses have been successful. The main aim of recent research is focused on the question what is primary mechanism leading to the molecular development of AD pathology. Promising explanation of triggering mechanism can be seen in vascular pathology that have direct influence on the development of pathological processes typical for Alzheimer disease. Novel insight into a number of cellular signaling mechanisms, as well as mitochondrial function in Alzheimer disease could also bring explanations of initial processes leading to the development of this pathology.

Department of Biochemistry Faculty of Science Masaryk University Brno Czech Republic

Comment In

Folia Neuropathol. 2014;52(2):205. PubMed

References provided by Crossref.org

ABCB1 Gene Polymorphisms and Their Contribution to Cognitive Decline in Mild Cognitive Impairment: A Next-Generation Sequencing Study

Serum PAI-1/BDNF Ratio Is Increased in Alzheimer's Disease and Correlates with Disease Severity

Polymorphism rs11867353 of Tyrosine Kinase Non-Receptor 1 (TNK1) Gene Is a Novel Genetic Marker for Alzheimer's Disease

Single Nucleotide Polymorphism rs11136000 of CLU Gene (Clusterin, ApoJ) and the Risk of Late-Onset Alzheimer's Disease in a Central European Population

CHAT gene polymorphism rs3810950 is associated with the risk of Alzheimer's disease in the Czech population

Association between 5q23.2-located polymorphism of CTXN3 gene (Cortexin 3) and schizophrenia in European-Caucasian males; implications for the aetiology of schizophrenia