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1.
Fig. 4

Fig. 4. Aβ deposition within higher-order olfactory regions. From: Olfactory Dysfunction Correlates with Amyloid-? Burden in an Alzheimer's Disease Mouse Model.

Coronal plate and quantification of Aβ deposition (% area, Thioflavin-S (Thio-S) and anti-Aβ (4G8)) in the (A) orbitofrontal cortex (OFC), (B) lateral entorhinal cortex (Eth), and (C) dorsal hippocampus (Hipp). Dashed regions within each coronal plate indicate approximate areas used for quantification.

Daniel W. Wesson, et al. J Neurosci. ;30(2):505-514.
2.
Fig. 3

Fig. 3. Aβ levels are distributed throughout PCX cell layers. From: Olfactory Dysfunction Correlates with Amyloid-? Burden in an Alzheimer's Disease Mouse Model.

(A) Coronal plates of the anterior (a-, top) and posterior piriform cortex (pPCX, bottom). Diagrams show the locations of cell layers i, ii and iii. Dashed lines indicate regions used for quantification in (B). Black boxes indicate approximate locations of images used in (B). (B) Representative Thioflavin-S (Thio-S) and anti-Aβ (4G8) staining in the aPCX (top) and pPCX (bottom) of Tg2576 mice at different age groups (mo=months). (C) Quantification of Aβ deposition (% area) within the PCX cortical layers (corresponding to arrangement in (B)).

Daniel W. Wesson, et al. J Neurosci. ;30(2):505-514.
3.
Fig. 2

Fig. 2. Anti-Aβ, but not Thio-S positive Aβ is deposited early in life within the olfactory bulb. From: Olfactory Dysfunction Correlates with Amyloid-? Burden in an Alzheimer's Disease Mouse Model.

(A) OB Coronal plate, indicating bulbar cell layers (glomerular (Gl), external plexiform (Epl), mitral/tufted (MT), Inner plexiform (Ipl) and granule cell (Grl)). (B) Representative Thioflavin-S (Thio-S) and anti-Aβ (4G8) staining in the olfactory bulbs of Tg2576 mice at different age groups (mo=months). (C) Quantification of Aβ deposition (% area) within the OB cell layers. (D) Pie charts comparing the average % area of Aβ deposition within each bulbar cell layer in aged (21–29mo old) Tg mice (n=6). Rarely were any fibrillar (Thio-S positive) Aβ deposits observed outside the Grl.

Daniel W. Wesson, et al. J Neurosci. ;30(2):505-514.
4.
Fig. 6

Fig. 6. Summary diagram showing the emergence of atypical olfactory behaviors in relation to Aβ deposition levels. From: Olfactory Dysfunction Correlates with Amyloid-? Burden in an Alzheimer's Disease Mouse Model.

(A) Aβ deposition (fibrillar (Thioflavin-S) and fibrillar and/or non-fibrillar (anti-Aβ)) in the olfactory bulb (OB, all layers) and piriform cortex (PCX, both anterior and posterior parts) in relation to olfactory behavioral performance throughout life in Tg2576 mice. Non-fibrillar Aβ levels within the OB were detectable at 3–4mo of age upon the start of impaired odor habituation. Atypical odor discrimination behaviors occur starting at 6–7mo of age. Abnormal odor investigation behavior did not begin until 16mo of age–prior to OB Aβ escalation. Data (depicted in approximate ‘levels’) are based upon the results displayed in Figs 1–4.

Daniel W. Wesson, et al. J Neurosci. ;30(2):505-514.
5.
Fig. 5

Fig. 5. Olfactory behaviors correlate with the spatio-temporal deposition of Aβ. From: Olfactory Dysfunction Correlates with Amyloid-? Burden in an Alzheimer's Disease Mouse Model.

(A) Pearson’s correlation values (r) between Aβ deposition (% area) within the olfactory bulb (OB), piriform cortex (PCX), orbitofrontal cortex (OFC), entorhinal cortex (Eth) and hippocampus (Hipp) and group-averaged olfactory scores (investigation time, % habituation, cross-habituation index (black circles in Fig 1C)) in Tg2576 mice. % habituation=the percentage difference between investigation duration in the first odor trial compared to the fourth. OB data=average of plaque area in granule cell layer. PCX data=average of aPCX and pPCX, all cell layers. Dashed line indicates threshold of statistical significance (r 0.36) based upon the population size within each bar (n=22 mice).

Daniel W. Wesson, et al. J Neurosci. ;30(2):505-514.
6.
Fig. 1

Fig. 1. Progressive and age-dependent emergence of AD-like atypical olfactory behavior in APP transgenic mice. From: Olfactory Dysfunction Correlates with Amyloid-? Burden in an Alzheimer's Disease Mouse Model.

Results from an odor cross-habituation test from 3–4, 6–7, 16 & 21–29mo old Tg2576 (Tg) and age-matched control mice (WT, see Methods for sample sizes). (A) Odor cross-habituation task design. Odors were presented by saturating an ‘odor stick’ with odor, placing this inside a hollow plastic tube, and inserting this into a stainless steel ‘odor port.’ Odors were presented in blocks of 4 successive trials (see Methods). (B) Investigation times for all trial #1 odor presentations. *p<.0001 Tg v. WT. (C) Odor habituation (normalized, see Methods) across 4 successive odor presentation trials (bars). Habituation difference (dots) indicate the difference between the genotypes (WT v. Tg) within each age-group in their % habituation across all 4 trials (see Methods). (D) Cross-habituation indices (discrimination) of Tg and WT mice. Cross-habituation index = the difference between the duration of the previous trial #4 odor investigation compared to that of the following trial #1 presentation. *p<.0001 Tg v. WT; All statistics are ANOVA followed by Fisher’s PLSD.

Daniel W. Wesson, et al. J Neurosci. ;30(2):505-514.

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