Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

Ex Input:
It is increasingly clear that the normal protein alpha-synuclein is in some manner closely associated with presynaptic components of select neuronal types within the adult human central nervous system (CNS) and, in addition, that in its pathologically altered state alpha-synuclein aggregates selectively in the form of filamentous inclusion bodies during certain progressive neurodegenerative disorders, such as familial and sporadic Parkinson's disease. By having the antibody AFshp raised specifically to alpha-synuclein to label Parkinson disease-specific Lewy bodies and Lewy neurites as well as synaptic boutons containing the unaltered protein, an initial attempt is made to map the overall distribution pattern and describe the staining behavior of the immunoreactive punctae in select regions of the prosencephalon. Neocortical immunolabeling is most prominent in the prodigious, but incompletely myelinated, association fields and faintest in the heavily myelinated primary motor and primary sensory fields, with the premotor and first order sensory association areas occupying an intermediate position. Of the thalamic grays evaluated, those containing powerfully myelinated fiber tracts (e.g. centrum medianum, habenular complex) show the weakest immunolabeling, whereas, less sturdily myelinated structures are highly immunoreactive. The fact that the immunostaining spectrum for normal alpha-synuclein is so broad, together with the fact that some thalamic sites actually are immunonegative leads to the following conclusions (1) alpha-synuclein, although present in the synaptic boutons of many nerve cells in the adult human CNS, is by no means ubiquitous there, and (2) neuronal types lacking the normal protein cannot generate the Parkinson's disease-specific filamentous pathology.

Ex Output:
Against which protein is the antibody used for immonostaining of Lewy bodies raised?

Ex Input:
Throughout its history, chronic myeloid leukemia (CML) has set precedents for cancer research and therapy. These range from the identification of the first specific chromosomal abnormality associated with cancer to the development of imatinib as a specific, targeted therapy for the disease. The successful development of imatinib as a therapeutic agent for CML can be attributed directly to decades of scientific discoveries. These discoveries determined that the BCR-ABL tyrosine kinase is the critical pathogenetic event in CML and an ideal target for therapy. This was confirmed in clinical trials of imatinib, with imatinib significantly improving the long-term survival of patients with CML. Continuing in this tradition of scientific discoveries leading to improved therapies, the understanding of resistance to imatinib has rapidly led to strategies to circumvent resistance. Continued studies of hematologic malignancies will allow this paradigm of targeting molecular pathogenetic events to be applied to many additional hematologic cancers.

Ex Output:
What tyrosine kinase, involved in a Philadelphia- chromosome positive chronic myelogenous leukemia, is the target of Imatinib (Gleevec)?

Ex Input:
Many of us believe that a person's mind becomes less active as he grows older.But this is not true,according to Dr.Lissy F.Jarvik,professor of psychiatry at the University of California,Los Angeles,and a board member of the New Center for Aging at the Veterans Hospital.She has studied the mental functioning of aging persons for several years.For example,one of her studies concerns 136 pairs of twins, who were first examined when they were already 60 years old.As Dr.Jarvik continued the study of the twins into their 70s and 80s,their minds did not generally decline as was expected. However,there was some decline in their psycho-motor speed. This means that it took them longer to accomplish mental tasks than it used to.But when speed was not a factor,they lost very little intellectual ability over the years.In general,Dr.Jarvik's studies have shown that there is no decline in knowledge or reasoning ability.This is true not only into the 30s and 40s,but into the 60s and 70s as well. As for learning new things,and ability to remember,studies by Dr.Jarvik and others show that the old are equal to the young.It is true that older people themselves often complain that their memory is not as good as it once was.However,much of what we call"loss of memory"is not that at a11. In the cases where the older person's mind really seems to decline,it is not necessarilv a sign of a decay due to becoming old or"senility".Often it is simply a sign of a depressed emotional state.This depression usually can be got rid of by counseling with a psychologist,or medicine which fights depression. In American society,when an older person loses something,we tend to call him or her"senile".But notice that when a younger person loses something,he does not blame it on senility or loss of memory.He finds some other excuse!

Ex Output:
A long-term study of 136 pairs of twins showed that the only factor that declined over the years was .