Molecular targets for cognitive improvement are a desirable context. This may lead to some improvement in a few dimensions of outcome in schizophrenia, assuming that cognitive deficits are a key component in its pathology, However we need not forget that they are neither universal nor unchallenged. It has been rightly pointed out that cognitive deficits may be the final result of many complex causations and pathways. No doubt succeeding in developing a molecule for working on molecular targets may give some benefit.

This entire research effort needs much appreciation. However, it opens other vistas of debate as well. E.g., cognition is a complex bio-behavioral psychological function. Believing that there are exclusive molecular targets suggests that ‘Cognitive deficits have molecular pathology.' That they are driven by dopaminergic, cholinergic, and glutaminergic neurotransmitter systems. Available data only shows association of dysfunction of these systems of neurotransmission in various areas of brain with cognitive deficits. It does not indicate what preceded and what...  Read more

Molecular targets for cognitive improvement are a desirable context. This may lead to some improvement in a few dimensions of outcome in schizophrenia, assuming that cognitive deficits are a key component in its pathology, However we need not forget that they are neither universal nor unchallenged. It has been rightly pointed out that cognitive deficits may be the final result of many complex causations and pathways. No doubt succeeding in developing a molecule for working on molecular targets may give some benefit.

This entire research effort needs much appreciation. However, it opens other vistas of debate as well. E.g., cognition is a complex bio-behavioral psychological function. Believing that there are exclusive molecular targets suggests that ‘Cognitive deficits have molecular pathology.' That they are driven by dopaminergic, cholinergic, and glutaminergic neurotransmitter systems. Available data only shows association of dysfunction of these systems of neurotransmission in various areas of brain with cognitive deficits. It does not indicate what preceded and what is the causal relationship. In that sense it would be quite premature to assume that molecular target medication development will provide any significant change in the scenario of outcome.

While the research attempt is commendable, it does not solve the problem of outcome in schizophrenia. E.g. Why do the patients having deficits and no deficits both go through a chronic deteriorating course? If cognition is a trait domain of schizophrenia, how is it that deficits will be reversed? Do we know the biological determinants of disability and dysfunction, and which is the main outcome concern? Is cognition anyway related to disability and dysfunction in schizophrenia?

Not speaking much about biology of memory, information processing, retention and learning in schizophrenia, the assumption discussed in the review seems itself premature. One would wonder if more architectural pharmacotherapies add to the basket of drugs or bring value to the patients.