Primary age‐related tauopathy (PART) and Alzheimer's disease (AD)

Bell et al. [1] recently compared neuropathologic, genetic, and cognitive profiles in 40 primary age-related tauopathy (PART) and 130 Alzheimer’s disease (AD) cases aged 85 years. PART, representing 22% of this consecutive oldest-old autopsy series, differed from classical AD by significantly slower rates of cognitive impairment, lower frequency of apolipoprotein E (APOE) ε4 (4.1% vs. 17.6%) but overrepresented APOE ε2 (12.2% vs. 5.3%), and significantly less extensive tau lesions beyond the medial temporal lobe, over 60% of definite PART subjects corresponding to Braak tau stage IV. Many of their findings are consistent with those observed in 144 cases with tau pathology in subjects aged 87.96 7.45 SD years, including 44 PART (30.5% of total), 71 classical AD and 29 “limbic” AD cases [2]. PART cases showed later onset, shorter duration, less severe cognitive impairment, significantly lower prevalence of APOE ε4 (3% vs. 38%), and over-representation of APOE ε2 (11% vs. 4%) [3,4]. In addition to absent or minimal amyloid b plaques (Thal scores 0-1) and virtually absent neuritic plaques but similar subcortical tau pathology [4], PART showed hippocampal tau pathology patterns differing from those in AD [2]. While 78%–85% of PART cases with Braak stages III and IV harbored greater (or equal) tau pathology in CA2 than CA1 sectors, AD showed reduced involvement of hippocampal sector CA2, increasing from Braak stage III to VI. Higher intensity of tau lesions in CA2 than in CA1 in 12% of our PART cases was similar to that in another recent autopsy study reporting milder involvement of CA2 at least in earlier or intermediate stages of AD [5]. These results are at variance to the