Heiko Braak

TL;DR: The intraneuronal accumulation of active cdc2 appeared to precede the deposition of PHF-tau phosphorylated at Ser 202/Thr 205 sites, consistent with the notion that cDC2 might be involved in the abnormal hyperphosphorylation of tau and consequently aggregation of t Tau into PHF at an early stage and that increased cdc1 activity is not consequent to the depositionof β-amyloid in AD brain.

TL;DR: It is proposed that a neurotropic pathogen enters the brain via two routes: nasal, with anterograde progression into the temporal lobe; and gastric, secondary to swallowing of nasal secretions in saliva, hence the term “dual hit.”

TL;DR: Interindividual differences in the distribution pattern of thalamic neurodegeneration indicate that the thalamus nuclei differ in their proclivities to degenerate in SCA2 and may suggest that they become involved at different phases in the evolution of the underlying degenerative process.

TL;DR: The use of 100’µm serial sections through the SCA2 patient's central somatosensory components showed that obvious neuronal loss occurred in nearly all of the relay stations of this system, which account for the somatomotor deficits that were observed in the young woman's impaired senses of vibration, position and temperature.

TL;DR: Altered neurofibrillary changes and brain β-amyloid can be stained selectively by silver impregnation on tissue sections and on sodium dodecyl sulfate-polyacrylamide gels, taking advantage of the physical development of nucleation sites, thereby permitting tight control of the entire procedure.