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Amyloid burden, cortical thickness, and cognitive function in the Wisconsin Registry for Alzheimer's Prevention.

Doherty BM, Schultz SA, Oh JM, Koscik RL, Dowling NM, Barnhart TE, Murali D, Gallagher CL, Carlsson CM, Bendlin BB, LaRue A, Hermann BP, Rowley HA, Asthana S, Sager MA, Christian BT, Johnson SC, Okonkwo OC - Alzheimers Dement (Amst) (2015)

Bottom Line: The Aβ+ group exhibited significant thinning of the entorhinal cortex and accelerated age-associated thinning of the parahippocampal gyrus compared with the Aβ- group.The Aβ+ group also had numerically lower, but nonsignificant, test scores on all cognitive measures, and significantly faster age-associated cognitive decline on measures of Speed & Flexibility, Verbal Ability, and Visuospatial Ability.Our findings suggest that early Aβ aggregation is associated with deleterious changes in brain structure and cognitive function, even in midlife, and that the temporal lag between Aβ deposition and the inception of neurodegenerative/cognitive changes might be narrower than currently thought.

View Article: PubMed Central - PubMed

Affiliation: Geriatric Research Education and Clinical Center, William S. Middleton Memorial VA Hospital, Madison WI ; Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI.

ABSTRACT

There is a growing interest in understanding how amyloid-β (Aβ) accumulation in preclinical Alzheimer's disease relates to brain morphometric measures and cognition. Existing investigations in this area have been primarily conducted in older cognitively-normal (CN) individuals. Therefore, not much is known about the associations between Aβ burden, cortical thickness, and cognition in midlife. We examined this question in 109, CN, late-middle-aged adults (mean age=60.72±5.65 years) from the Wisconsin Registry for Alzheimer's Prevention. They underwent Pittsburgh Compound B (PiB) and anatomical magnetic resonance (MR) imaging, and a comprehensive cognitive exam. Blinded visual rating of the PiB scans was used to classify the participants as Aβ+ or Aβ-. Cortical thickness measurements were derived from the MR images. The Aβ+ group exhibited significant thinning of the entorhinal cortex and accelerated age-associated thinning of the parahippocampal gyrus compared with the Aβ- group. The Aβ+ group also had numerically lower, but nonsignificant, test scores on all cognitive measures, and significantly faster age-associated cognitive decline on measures of Speed & Flexibility, Verbal Ability, and Visuospatial Ability. Our findings suggest that early Aβ aggregation is associated with deleterious changes in brain structure and cognitive function, even in midlife, and that the temporal lag between Aβ deposition and the inception of neurodegenerative/cognitive changes might be narrower than currently thought.

No MeSH data available.


Related in: MedlinePlus

Amyloid beta (Aβ) burden accelerates age-related cognitive decline. The plots depict predicted values derived from the regression equation (circles), with the line of best linear fit overlaid. Red circles/line = Aβ+ group, blue circles/line = Aβ− group.
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fig3: Amyloid beta (Aβ) burden accelerates age-related cognitive decline. The plots depict predicted values derived from the regression equation (circles), with the line of best linear fit overlaid. Red circles/line = Aβ+ group, blue circles/line = Aβ− group.

Mentions: Results of the main effect of Aβ on cognition are summarized in Table 3. The Aβ+ group exhibited numerically lower scores on all six cognitive factors relative to the Aβ− group. However, these differences did not meet our criterion for statistical significance (Ps >.1). With respect to the Aβ-induced acceleration of age-related cognitive decline, we found that Aβ+ participants demonstrated significantly greater age-associated cognitive decline on Speed & Flexibility (age*Aβ rating P =.034), and also showed trends for a faster rate of age-associated cognitive decline on Verbal Ability and Visuospatial Ability (age*Aβ rating Ps =.058 and .089, respectively). These results are shown in Fig. 3.


Amyloid burden, cortical thickness, and cognitive function in the Wisconsin Registry for Alzheimer's Prevention.

Doherty BM, Schultz SA, Oh JM, Koscik RL, Dowling NM, Barnhart TE, Murali D, Gallagher CL, Carlsson CM, Bendlin BB, LaRue A, Hermann BP, Rowley HA, Asthana S, Sager MA, Christian BT, Johnson SC, Okonkwo OC - Alzheimers Dement (Amst) (2015)

Amyloid beta (Aβ) burden accelerates age-related cognitive decline. The plots depict predicted values derived from the regression equation (circles), with the line of best linear fit overlaid. Red circles/line = Aβ+ group, blue circles/line = Aβ− group.
© Copyright Policy - CC BY-NC-ND
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4492165&req=5

fig3: Amyloid beta (Aβ) burden accelerates age-related cognitive decline. The plots depict predicted values derived from the regression equation (circles), with the line of best linear fit overlaid. Red circles/line = Aβ+ group, blue circles/line = Aβ− group.
Mentions: Results of the main effect of Aβ on cognition are summarized in Table 3. The Aβ+ group exhibited numerically lower scores on all six cognitive factors relative to the Aβ− group. However, these differences did not meet our criterion for statistical significance (Ps >.1). With respect to the Aβ-induced acceleration of age-related cognitive decline, we found that Aβ+ participants demonstrated significantly greater age-associated cognitive decline on Speed & Flexibility (age*Aβ rating P =.034), and also showed trends for a faster rate of age-associated cognitive decline on Verbal Ability and Visuospatial Ability (age*Aβ rating Ps =.058 and .089, respectively). These results are shown in Fig. 3.

Bottom Line: The Aβ+ group exhibited significant thinning of the entorhinal cortex and accelerated age-associated thinning of the parahippocampal gyrus compared with the Aβ- group.The Aβ+ group also had numerically lower, but nonsignificant, test scores on all cognitive measures, and significantly faster age-associated cognitive decline on measures of Speed & Flexibility, Verbal Ability, and Visuospatial Ability.Our findings suggest that early Aβ aggregation is associated with deleterious changes in brain structure and cognitive function, even in midlife, and that the temporal lag between Aβ deposition and the inception of neurodegenerative/cognitive changes might be narrower than currently thought.

View Article: PubMed Central - PubMed

Affiliation: Geriatric Research Education and Clinical Center, William S. Middleton Memorial VA Hospital, Madison WI ; Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI.

ABSTRACT

There is a growing interest in understanding how amyloid-β (Aβ) accumulation in preclinical Alzheimer's disease relates to brain morphometric measures and cognition. Existing investigations in this area have been primarily conducted in older cognitively-normal (CN) individuals. Therefore, not much is known about the associations between Aβ burden, cortical thickness, and cognition in midlife. We examined this question in 109, CN, late-middle-aged adults (mean age=60.72±5.65 years) from the Wisconsin Registry for Alzheimer's Prevention. They underwent Pittsburgh Compound B (PiB) and anatomical magnetic resonance (MR) imaging, and a comprehensive cognitive exam. Blinded visual rating of the PiB scans was used to classify the participants as Aβ+ or Aβ-. Cortical thickness measurements were derived from the MR images. The Aβ+ group exhibited significant thinning of the entorhinal cortex and accelerated age-associated thinning of the parahippocampal gyrus compared with the Aβ- group. The Aβ+ group also had numerically lower, but nonsignificant, test scores on all cognitive measures, and significantly faster age-associated cognitive decline on measures of Speed & Flexibility, Verbal Ability, and Visuospatial Ability. Our findings suggest that early Aβ aggregation is associated with deleterious changes in brain structure and cognitive function, even in midlife, and that the temporal lag between Aβ deposition and the inception of neurodegenerative/cognitive changes might be narrower than currently thought.

No MeSH data available.


Related in: MedlinePlus