When I started my training in neuropathology almost 20 years ago, I was slightly disappointed by the rather small number of neurodegenerative autopsy cases. Instead, at that time, cerebral ischemia represented the focus of investigation at this laboratory. These days, however, I Wnd it surprising that ischemia research appears to vanish in the realm of neuropathology. Neurodegenerative diseases are certainly frequent and literally represent the core of neuropathology. Furthermore, tumor biopsy cases, despite their rare total incidence, are undoubtedly of major importance of how modern neuropathology deWnes itself. Nevertheless, the mere look at the huge number of patients dying from cerebral ischemia, both global and focal,—as, e.g., seen after cardiac arrest or ischemic stroke, respectively—renders the latter the most common group of diseases where the brain is involved. Consider the following facts when taking only stroke into account, which is ischemic in about 85% of cases [10]: Wrst, stroke ranks third among all causes of death in industrial countries, i.e., right after heart disease and cancer. Second, in the United States, on average every 45 s someone suVers a stroke and every 3–4 min someone dies of it. Third, in the long term, 50–70% of stroke survivors regain functional independence, whereas 15–30% remain permanently disabled, and 20% require institutional care at 3 months of onset [1]. Considering the frequency of cerebrovascular disease compared to the factual lack of speciWc therapies (except for recanalization of the occluded vessel after stroke which, however, is only possible for a low percentage of patients)—this situation should provide a strong incentive to further enhance research activities. In this context, cerebral ischemia oVers a fascinating opportunity to study both neurodegenerative and neuroregenerative processes. Re-focusing on stroke, it has been well known to clinicians for decades that consistent, albeit slow and incomplete spontaneous recovery often takes place over time [12]. The underlying processes regulating the beneWcial reaction of the CNS in response to injury or physiological demands have been designated plasticity phenomena and describe the potential of the brain for adaptive changes [4]. By means of modern imaging techniques, it has become clear over the past years that there is no Wxed correspondence between speciWc brain areas and speciWc body parts. Instead, changes in peripheral organs or environmental inXuences may modify the brain throughout life [9]. Some examples may illustrate this impressive cerebral capacity. Using structural MRI, Maguire and colleagues could demonstrate that the posterior hippocampi of London taxi drivers were larger compared to those of controls. Furthermore, the hippocampal volume correlated with the amount of time spent as a taxi driver [8]. Similarly, extensive studying by medical students for their medical examination was associated with an increase in the volume of the posterior hippocampus as shown by voxel-based morphometry based on high-resolution MRI [6]. Bilateral expansion of the grey matter in the mid-temporal area and the left posterior intraparietal sulcus were observed in inexperienced persons subjected to learn juggling [5]. It is certainly not surprising that there is also a genetic background for the possible extent of brain plasticity as previously demonstrated by a BDNF val66met polymorphism, which distinctly modiWes experience-dependent plasticity in the human motor cortex [7]. In this context, it should be mentioned that the met allele of this polymorphism is also C. Sommer (&) Department of Neuropathology, Mainz University Medical Center, Langenbeckstrasse 1, 55131 Mainz, Germany e-mail: sommer@neuropatho.klinik.uni-mainz.de