Duration of neurofibrillary changes in the hippocampal pyramidal neurons

TL;DR: The data suggest that tauopathy associated with sporadic Alzheimer disease may begin earlier than previously thought and possibly in the lower brainstem rather than in the transentorhinal region.

TL;DR: Findings may indicate that the Alzheimer’s disease-related pathological process leading to neurofibrillary tangle formation does not begin in the cerebral cortex but, rather, in select subcortical nuclei, and it may start quite early, i.e., before puberty or in early young adulthood.

TL;DR: The idea of possible disease progression from the locus coeruleus to the transentorhinal region of the cerebral cortex via neuron-to-neuron transmission and transsynaptic transport of tau protein aggregates is discussed, and it is speculated that such a mechanism together with the very long prodromal period that characterizes Alzheimer's disease may be indicative of a prion-like pathogenesis for this tauopathy.

TL;DR: This review emphasizes the importance of preserving synaptic structure and function in AD by administering “synaptoprotection” therapy, which will probably need to be administered at a critical early time point, perhaps years before onset of clinical symptoms.

TL;DR: The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations, permitting the differentiation of six stages.

TL;DR: It is suggested that tau in Alzheimer brain is an abnormally phosphorylated protein component of PHF, the two major locations of paired-helical filaments in Alzheimer disease brain.

TL;DR: Antisera raised against synthetic peptides corresponding to these different human tau isoforms demonstrate that multiple tau protein isoforms are incorporated into the neurofibrillary tangles of Alzheimer's disease.

TL;DR: Examination of temporal lobe structures from Alzheimer patients reveals a specific cellular pattern of pathology of the subiculum of the hippocampal formation and layers II and IV of the entorhinal cortex that isolates the hippocampus from much of its input and output and probably contributes to the memory disorder in Alzheimer patients.