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ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
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Review Article

Recent Developments in Treating Alzheimers Disease

Eva Zerovnik1,2*, Natasa Kopitar Jerala1 and Robert Layfield3

1Department of Biochemistry and Molecular and Structural Biology, Jožef Stefan Institute, 1000 Ljubljana, Slovenia

2CipKeBip - Center of Excellence for Integrated Approaches in Chemistry and Biology of Proteins, 1000 Ljubljana, Slovenia

3University of Nottingham, Medical School, Queen’s Medical Centre, Nottingham NG7 2UH, UK

Corresponding Author:
Eva Zerovnik
Department of Biochemistry and Molecular and Structural Biology
Jozef Stefan Institute, 1000 Ljubljana, Slovenia
Tel: 386-147-73753
E-mail: [email protected]

Received date: January 19, 2016; Accepted date: March 11, 2016; Published date: March 18, 2016

Citation: Zerovnik E, Jerala NK, Layfield R (2016) Recent Developments in Treating Alzheimer’s Disease. J Alzheimers Dis Parkinsonism 6:220. doi: 10.4172/2161-0460.1000220

Copyright: © 2016 Zerovnik E, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Early diagnosis and efficient treatment for sporadic Alzheimer’s disease (AD) are urgently needed as the condition becomes an increasing burden within aging societies. We collected recent data on the progress towards effective treatments of AD, from targeting Aβ aggregation, passive immunization with anti-Aβ antibodies, fighting acute and chronic inflammation, modulating autophagy to balancing metals ions. We argue that from successful model studies and pre-clinical trials, insights into the critical pathogenic mechanisms at the molecular and cellular levels are confirmed. They in one way or another seem to support the modified amyloid cascade hypothesis, in which Aβ oligomers are believed to impair intracellular membranes, possibly resulting in mitochondrial and lysosomal dysfunctions that may lead to oxidative stress and impairment in protein clearance by autophagy, respectively. In accordance, chronic inflammation due to activation of microglia, is also consistently observed in AD brains.

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