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Patients with behavioral variants of Alzheimer's disease (bvAD, formerly known as "frontal AD") may experience prominent behavioral symptoms and personality changes at an early stage, such as inhibition, compulsive behavior, and loss of compassion
.
These people are clinically reminiscent of behavioral variant frontotemporal dementia (bvFTD), but with AD as the main pathological feature, they are neuroanatomically similar to "typical" AD (tAD) patients because of the atrophy and low of bvAD The metabolic pattern mainly occurs in the temporal parietal area
Imaging and pathological investigations (mainly case reports or small cohort studies with low incidence based on this phenotype) provide mixed results on the involvement of the frontal cortex in bvAD
In this way, Ellen Singleton and others of the University of Amsterdam explored the regional distribution of tau pathology in bvAD: using positron emission tomography (PET) and autopsy, the distribution of tau deposition in bvAD in vivo and in vitro was investigated
.
For the PET study of tau, 7 amyloid β-positive bvAD patients received [18F]flortaucipir or [18F]RO948 PET
.
They converted the tau PET uptake value into a standardized (W-) score, and adjusted the mini mental status check of the AD group (n=205) where age, gender, and "typical" memory were predominant
W-scores are calculated in the medial, temporoparietal, medial and lateral forehead, insula and regions of interest in the whole brain, frontal to medial and frontal to parietal ratios, and intrinsic functional connection network templates
.
In postmortem studies, the percentage of AT8 (tau) positive areas in hippocampal CA1, temporal lobe, parietal lobe, frontal lobe, and insular cortex were confirmed by autopsy in bvAD (n=8) and typical AD (tAD; n=7) Compare between patients
.
They found that W-scores≥1.
96 (equivalent to P<0.
05) in individual areas were observed in three cases, namely case No.
5: medial prefrontal cortex (W=2.
13) and anterior default mode network (W=3.
79), Case No.
2: lateral prefrontal cortex (W=2.
79) and saliency network (W=2.
77), and case No.
7: frontal lobe and thalamic ratio (W=2.
04)
.
The remaining 4 cases belonged to the normal distribution range of the tAD group
AT8 staining at autopsy showed that there was no group-level regional difference in phosphorylated tau levels between bvAD and tAD (all P>0.
05)
.
The important significance of this study is that, whether in vivo or in vitro, bvAD patients show a heterogeneous distribution of tau pathology
.
Since the key areas involved in behavior regulation are not always disproportionately affected by tau pathology, other factors are more likely to drive the clinical phenotype of bvAD
Whether in vivo or in vitro, bvAD patients show a heterogeneous distribution of tau pathology.
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