Dementia is a clinical syndrome that can be caused by multiple conditions, with variable speed of onset, rate of evolution, and duration. Some of these conditions are relentlessly progressive and ultimately fatal, some are treatable, and a few are reversible. Approximately 10% of patients are categorized as having treatable dementias, with normal pressure hydrocephalus (NPH), chronic subdural hematoma, and slow growing brain tumors being the most common etiologies. Idiopathic NPH is a typical treatable form of dementia. The invasive and non-invasive tests of cerebrospinal fluid (CSF) dynamics and drainage can provide an improved measure of postoperative outcomes. However, there is no evidence that testing is superior to clinical examination. Therefore, we should be cautious when excluding patients from shunting based on testing. Two changes in CSF circulatory physiology have been noted as part of ageing. CSF production and turnover are further diminished in patients with Alzheimer's disease (AD) and idiopathic NPH. Poor CSF clearance of proteins, such as Tau and beta amyloid, may play a role in the progression of AD. Improving CSF drainage by shunt can enhance the extracellular clearance of end products of oxidative reactions and lower brain lipid peroxidation. Recently, some efforts for treating AD have been reported. Altering the brain micro-environment to foster appropriate maturation of graft-derived neurons may be critical for improving the efficacy of neural stem cell transplantation therapy for AD. Neuroanatomic circuits mediating memory are accessible and the function of memory circuits can be modulated with neurostimulation, such as deep brain stimulation (DBS) and vagal nerve stimulation. We may identify therapeutic implications for patients with memory disorders. Such studies provide the proof of principle that DBS may remotely activate neocortical structures to enhance memory performance.