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Background  A substantial number of patients clinically diagnosed with Alzheimer’s disease do not harbor amyloid pathology. We analyzed the presence and extent of tau deposition and neurodegeneration in amyloid-positive (AD) and amyloid-negative (nonAD) ADNI subjects while also taking into account age of onset (< or > 65 years) as we expected that the emerging patterns could vary by age and presence or absence of brain amyloidosis.    Methods  One hundred and ten early-onset AD (EOAD), 121 EOnonAD, 364 late-onset AD (LOAD), and 175 LOnonAD mild cognitive impairment (MCI) and dementia (DEM) subjects were compared to 291 ADNI amyloid-negative control subjects using voxel-wise regression in SPM12 with cluster-level family-wise error correction at  p  FWE  < 0.05). A subset of these subjects also received  18 F-flortaucipir scans and allowed for analysis of global tau burden.    Results  As expected, relative to LOAD, EOAD subjects showed more extensive neurodegeneration and tau deposition in AD-relevant regions. EOnonAD MCI  showed no significant neurodegeneration, while EOnonAD DEM  showed bilateral medial and lateral temporal, and temporoparietal hypometabolism. LOnonAD MCI  and LOnonAD DEM  showed diffuse brain atrophy and a fronto-temporo-parietal hypometabolic pattern. LOnonAD and EOnonAD subjects failed to show significant tau binding.    Conclusions  LOnonAD subjects show a fronto-temporal neurodegenerative pattern in the absence of tau binding, which may represent underlying hippocampal sclerosis with TDP-43, also known as limbic-predominant age-related TDP-43 encephalopathy (LATE). The hypometabolic pattern observed in EOnonAD DEM  seems similar to the one observed in EOAD MCI . Further investigation into the underlying etiology of EOnonAD is warranted.

Neurodegenerative changes in early- and late-onset cognitive impairment with and without brain amyloidosis