In more recent years (late 1980s), actually, the opposite hypothesis has been formulated.
The hypothesis has been formulated that, in the context of evolving epilepsy, pathological transsynaptic activation of NMDA receptors leads to increased MMP-9 transcription via ERK1/2 and/or PI3 kinase-dependent mechanisms [8].
This hypothesis has been formulated also for other neurodegenerative diseases related to protein misfolding and aggregation, such as Parkinson's and Alzheimer's diseases and the transmissible spongiform encephalopathies.
For each of the factors mentioned, a hypothesis has been formulated and measures have been selected.
The following research hypothesis has been formulated: "There are differences in the functioning in elderly between the two study groups".
This hypothesis has been formulated mainly for viruses, although it has been not excluded that also bacteria and fungi could be involved.
Additionally, the hypothesis has been formulated that VEGF supports tumor growth and progression by acting directly through VEGFRs expressed on tumor cells.
On the one hand, the hypothesis has been formulated that AD is an inevitable manifestation of senescence in that the disease, with its neuropathological signatures, is considered a normal phenomenon of aging [ 9].
A captivating bioengineering hypothesis has been formulated in recent times by Uri Galili in order to favour an immediate regeneration and hence avoid rejection mediated by non-gal antibodies.
This approach is therefore useful for biologists to identify gaps between the hypothesized mechanistic description of a pathway of interest, and the experimental data on which the hypothesis has been formulated.
