Format

Send to

Choose Destination
See comment in PubMed Commons below
Expert Opin Ther Targets. 2011 May;15(5):535-55. doi: 10.1517/14728222.2011.557363. Epub 2011 Feb 11.

Neurobiological aspects of Alzheimer's disease.

Author information

  • 1Pharmacology Research Laboratory, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, India. dr_chopra_k@yahoo.com

Abstract

INTRODUCTION:

The molecular pathogenesis of Alzheimer's disease (AD) includes a variety of risk factors, extracellular deposition of β-amyloid, accumulation of intracellular neurofibrillary tangles, oxidative neuronal damage and inflammatory cascades. Although amyloid-β-containing senile plaques and phospho-tau-containing neurofibrillary tangles are hallmark lesions of AD, neither is specific to nor even a marker of the disease. From a biochemical point of view the most consistent finding is a decreased level of choline acetyltransferase. In recent years, cumulative evidence has been gained on the involvement of neuronal lipoprotein activity, and on the role of cholesterol and other lipids in pathogenesis. Although basic research has made remarkable progress in the past two decades, currently available drugs are only able to improve cognitive symptoms temporarily and no treatment can reverse, stop or even slow this inexorable neurodegenerative process.

AREAS COVERED:

The various neurobiological events associated with development of AD and the multiple treatment approaches for combating this disorder.

EXPERT OPINION:

AD is a complex multifactorial disorder and thus a single target or pathogenic pathway is unlikely to be identified. Developing therapeutic interventions demands a greater understanding of the processes and the differential involvement of the various mediators. Effective therapeutics are urgently needed, and it is hoped that anti-amyloid strategies will offer a significant step towards a causal therapy.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Write to the Help Desk