Tuesday, May 15, 2012

A Possible Cause of Colony Collapse Disorder in Honey Bees

The phenomenon of colony collapse disorder (CCD) in honey bees is a recent one that has plagued honey bee populations in North America.  CCD is a recent condition  that is characterized by the disappearance of honey bees from the hive.  This has long puzzled investigators.  A number of different causes have been proposed including pesticides, microbial or parasitic infection and environmental degradation.
Since honey bees significantly contribute to plant propagation through pollination, It is important to uncover the actual cause of CCD so that this situation can be addressed and remedied.  Of the possible candidates as cited above, pesticides have long been suspected of playing a leading role.   Farming practices often involve the wide use of systemic pesticides.  Systemic  agents permeate all the tissues of a plant ultimately contaminating the nectar and pollen on which the bees rely.  In addition, honey bees heavily utilize common blooming crops including oilseed rape, maize and sunflower that are commonly exposed to pesticides.
Although pesticide manufacturers are required to monitor the mortality of unintended life forms in the field, there is growing evidence that sub lethal doses may adversely impact behavioral problems in aging honey bees especially in regard to navigational skills.  There is a class of insecticides, the so-called, "Neonicotinoids" routinely used to protect crops against aphids that are strong candidates for having an adverse impact upon honey bees.  The reason for this possible connection is that pesticides of this class selectively bind to nicotinic acetylcholine receptors that are essential for a properly functioning nervous system in insects.
Dr. Mickael Henry and his colleagues from the Institut de la Recherche Agronomique in Avignon, France have shown that, "nonlethal exposure of honey bees to thiamethoxam (neonicotinoid systemic pesticide) causes high mortality due to homing failure at levels that put a colony at risk of collapse."
This finding is of crucial importance, for it provides direct evidence of the actual causative agent in CCD.  These finding should provide impetus for a reexamination of the widespread use of nonicotinoid pesticides that are currently in worldwide use.

Wednesday, May 2, 2012

An Existing Drug May Offer Promise for Patients with Alzheimer’s Disease

Dr Cramer and her colleagues at Case Western Reserve University School of Medicine in Cleveland have discovered that the drug called bexarotene reverses the degenerative effects in the brains of mice that suffer the equivalent of Alzheimer's disease found in humans.
In the brain of Alzheimer's patients the most predominant anomaly is the presence of what is referred to as neuritic plaques and neurofibrillary tangles which are believed to lead to the disruption of normal brain activity and cell death that ultimately robs patients of the ability to remember and use reasoned judgment.  The disease process proceeds at a slow and ultimately deadly pace.
The underlying mechanism for the disease remains elusive though there are numerous hypotheses that have been proposed to explain disease onset.  What is well established, however, is the fact that the plaques result from the aggregation of the peptide – β-Amyloid (Aβ) - a peptide is a relatively small molecule made of a sequence of amino acids analogous to the structure of proteins.  Aβ is a direct product of the fragmentation of a trans-membrane protein called amyloid precursor protein (APP).  Trans-membrane proteins span the plasma membrane that encircles every cell.  There is a protein complex associated with the cleavage of APP; one of the proteins in this complex is an enzyme, protease – γ – secretase; this enzyme is a necessary component for the effective cleavage of APP. 
Furthermore, the modification   – mutation –  of three genes have been implicated in the autosomal-dominant form of Alzheimer's disease.  These genes are responsible for the production of APP and two additional factors required for the function of protease – γ – secretase .
Aggregates of the Aβ peptide are suspected of causing dementia, as mentioned earlier, possibly by interfering with the appropriate communication between neighboring neurons in the areas of the brain affected.  In spite of the ambiguity surrounding the exact etiology of Alzheimer's disease, the genetic association is unambiguous.  For example, individuals with a single copy of the APOE-4 gene have a five-fold increased risk of contracting the illness.
Of great interest is the fact that Cramer and her associates have shown that administration of the drug bexarotene to mice with the murine version of Alzheimer's disease results in the increased expression of APO-E – a protein that is known to bind to Aβ, the subsequent rapid clearance of Aβ  and , most importantly, the reversal of abnormal behavior in the diseased animals.
These findings are of immense interest.  Whether or not these results can translate into effective treatment of human Alzheimer's patients is dependent upon extensive and carefully executed clinical trials given the many differences between the architecture of the human and mouse brain.  There is, however, a cause for hope.