You have now left the main British Psychological Website - return to the main site >>
  Back to the Main BPS Site
Home
Return to Main BPS Site

You Are Here: Home > Conference Proceedings > 2007 Psychobiology 22nd Annual Scientific Meeting > Scopolamine model of dementia: Validation against [...]

 
 

Conference Proceedings

Abstract Details

 

2007 Psychobiology 22nd Annual Scientific Meeting


Conference Venue: Low Wood Hotel, Lake Windermere
Psychobiology Section

From: 03 Sep 2007
To: 05 Sep 2007
 
 
Poster(s)

Scopolamine model of dementia: Validation against cognitive performance and clinical ratings using an effect size model

C. Deeprose
Cognitive Drug Research

C. Edgar
Cognitive Drug Research

I.D. Marshall
Cognitive Drug Research

A. Embleton
Cognitive Drug Research

B.K. Saxby
Cognitive Drug Research

K.A. Wesnes
Cognitive Drug Research


Introduction
Single doses of the anticholinergic drug scopolamine produce marked but reversible impairments to cognition in healthy volunteers. These temporary deficits are similar to those seen in disease states related to cholinergic dysfunction, such as Alzheimer’s disease. We used an effect size methodology to directly compare the magnitude of impairment to cognition seen with scopolamine to that seen with stratification of disease severity using the Mini Mental State Examination (MMSE) and Global Deterioration Scale (GDS).

Methods
The Cognitive Drug Research (CDR) normative database was used to calculate effect sizes for impairment on the core cognitive domains of attention, working memory and episodic secondary memory with administration of 0.4, 0.5, 0.6, 0.7 and 0.8 mg subcutaneous scopolamine in healthy volunteers. These were compared to effect sizes calculated for cognitive impairment seen for ‘mild’, ‘mild–moderate’ and ‘moderate’ Alzheimer’s disease states as compared to age matched controls and for ratings on the MMSE and GDS.

Results
The effect size methodology permitted direct comparison of data on five domains from the CDR system between scopolamine and the disease states, MMSE and GDS ratings. The data indicated dose dependent impairment to cognition with scopolamine, and disease severity incrementing impairments on the stages and scales. The patterns of impairment with scopolamine over the domains will be contrasted to the patterns of impairment seen in the stratified dementia states.

Conclusions
Scopolamine models the cognitive impairments in Alzheimer’s disease on various cognitive domains including the ability to focus and sustain attention, to hold information in working and episodic memory and the time taken to retrieve information from memory. The domain on which scopolamine most underestimates the impairments in Alzheimer’s disease is the speed of retrieval of information from working and secondary memory.


 


 

Back to Conference Details

 
Contact Details | Privacy | Legal | Accessibility |
^ Top of Page