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1. Tau decays into two mesons: an overview

   https://doi.org/10.1051/epjconf/201921208003  

   Gonzàlez-Solís, Sergi (January 2019, EPJ Web of Conferences)

   Achasov, M.N.; Ignatov, F.V.; Krokovny, P.P. (Ed.)

   We review the state-of-the-art theoretical analyses of tau decays into a pair of mesons and a neutrino. The participant vector and scalar form factors, f + ( s ) and f 0 ( s ), are described in the frame of Chiral Perturbation Theory with resonances supplemented by dispersion relations, and the physical parameters of the intermediate resonances produced in the decay are extracted through the pole position of f +,0 ( s ) in the complex plane. As a side result, we also determine the low-energy observables associated to the form factors. We hope our study to be of interest for present and future experimental analyses of these decays. 

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2. A Two-Species Model for Abnormal Tau Dynamics in Alzheimer’s Disease

   https://doi.org/10.1007/978-3-031-47425-5_7  

   Wen, Zheyu; Ghafouri, Ali; Biros, George (January 2023, Springer Nature Switzerland)
3. Extracellular Tau Oligomers Damage the Axon Initial Segment by an Endogenous Tau‐Dependent Mechanism

   https://doi.org/10.1002/alz.078491  

   Best, Merci N; Lim, Yunu; Ferenc, Nina; Kim, Nayoung; Wang, Dora Bigler; Sharifi, Kamyar; Wasserman, Anna; McTavish, Sloane; Siller, Karsten; Jones, Marieke K; et al (December 2023, Alzheimer's & Dementia)

   Abstract BackgroundNeuronal polarity and synaptic connectivity are compromised in Alzheimer’s disease (AD) and other tauopathies. The axon initial segment (AIS) is a key structure for regulating polarity and functions of neurons. It occupies the first 20‐60 µm of the axon, comprises a diffusion barrier that segregates axon‐enriched from somatodendritic‐enriched molecules, and has a high concentration of voltage‐gated ion channels that generate action potentials. Extracellular amyloid‐β oligomers compromise AIS integrity. However, effects on the AIS of toxic tau species, including extracellular oligomers (xcTauOs) that spread tau pathology from neuron to neuron by a prion‐like process, whereas unknown. Therefore, we wanted to test the hypothesis that AIS structure is sensitive to xcTauOs. MethodPrimary cortical neurons derived from either wild type (WT), or tau knockout (KO) mice were exposed to xcTauOs or vehicle. Quantitative western blotting and immunofluorescence microscopy with an antibody against the AIS‐enriched protein TRIM46 was used to monitor effects on the AIS. The same methods were also used to compare TRIM46 and two other AIS proteins, ankyrin‐G and neurofascin‐186 in human hippocampal tissue obtained from AD and age‐matched non‐AD donors. ResultIn cultured WT, but not TKO neurons, xcTauOs cause a trend toward AIS shortening and reduce the concentration of the resident AIS protein, TRIM46, without affecting total TRIM46 levels. Lentiviral‐driven human tau expression in tau KO neurons rescues TRIM46 sensitivity to xcTauOs. In human AD hippocampus, AIS length and TRIM46 concentration within the AIS are reduced in neurons containing neurofibrillary tangles (NFTs), without affecting the overall protein levels of multiple resident AIS proteins. ConclusionThese collective findings demonstrate that in cultured neurons, xcTauOs cause partial AIS damage by a mechanism dependent on intracellular tau, thereby raising the possibility that AIS reduction in AD is caused by xcTauOs working in concert with endogenous neuronal tau. 

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4. A measurable angular distribution for $$ \overline{B}\to {D}^{* }{\tau}^{-}{\overline{v}}_{\tau } $$ ​decays.

   https://doi.org/https://doi.org/10.1007/JHEP07(2020)194  

   Bhubanjyoti Bhattacharya, Alakabha Datta (July 2020, Journal of high energy physics)

   null (Ed.)
5. Effective equidistribution and property $$(\tau )$$

   https://doi.org/10.1090/jams/930  

   Einsiedler, M.; Margulis, G.; Mohammadi, A.; Venkatesh, A. (January 2020, Journal of the American Mathematical Society)