14, 15 Higher levels of CSF Tau are associated with elevated brain Tau levels, 13, 16 and with the progression of AD. 17– 19 Therefore, higher CSF Tau to A β42 ratio 20 or lower CSF A β42 to Tau ratio 21 can distinguish AD patients from healthy controls and predict the development of AD (reviewed in ref. 22).
10– 12 In vivo identification of brain A β has become increasingly important due to the development of novel AD drugscite ref 3 here, which are likely to be effective only in patients with A β pathology, and maybe only in early disease stage, when a correct clinical diagnosis of AD is difficult to make.
Thirteen plant tissues were selected to represent the major stages of wheat development and to mirror the experiment of Ref. [ 27] for barley (cv. Morex).
Nevertheless, these protein oxidation signals were used in different sensors (reviewed in ref (210)) and for the development of various biomarker sensors (reviewed in refs (211) and (212)).
Orthologues of sarcoglycan genes have also been identified in zebrafish, which represent an established model of vertebrate development (Ref. 70).
Binding of thalidomide to the CRBN complex and inhibition of CRBN E3 ligase activity appear to be the underlying molecular mechanisms for thalidomide-induced teratogenicity by the perturbation of embryonic development (Ref. 94).
Acetylation of transcription factors can either stimulate or silence gene transcription, and inappropriate acetylation levels have been associated with aberrant transcription of disease-promoting genes in cancer and inflammation, instigating the development of inhibitors for histone deacetylases (HDACs) (Ref. 7) and histone acetyltransferases (HATs) (Ref. 8).
The developmental history of tectal organization is also of interest; in fact, frogs and fishes were the early model animals for the study of the development of retinotectal projections (eg. refs. [11] [14]).
However, the development of specific hypothesis tests (e.g., ref. [2]) showed that the molecular clock is too often untenable [3].
Studies in obesity, type 2 diabetes, and gestational diabetes mellitus (GDM) suggest that the deficiency of AdpN triggers the progression to insulin resistance and the development of metabolic inflammation (recently reviewed in ref. 6).
Interestingly, and in contrast, novel data suggest that B cells may play an important role in allograft survival and the development of operational transplant tolerance (reviewed in Ref. 3).
