Construction of supramolecular self-assemblies whose self-assembling process and self-assembled architectures can be controlled by external stimuli is a fascinating and challenging topic for supramolecular chemists. The modification of photochromic molecules with noncovalent interaction sites or the incorporation of photochromic molecules into self-assembling modules makes light an ideal external input, providing high-performance photoresponsive multicomponent self-assemblies. Among such systems, in this tutorial review we deal with several photoresponsive supramolecular self-assemblies showing a unique mechanism and/or type of photoresponse. These examples illustrate that we would be able to produce further new photoresponsive molecular ensembles if one can elaborately hybridize photochromic molecules to specifically-designed supramolecular self-assemblies. We believe that the accumulation of insight into the construction principle, mechanism and concept of such smart supramolecular self-assemblies should realize practical smart functional materials.

Increasing evidence suggests that vascular risk factors contribute to neurodegeneration, cognitive impairment and dementia. While there is considerable overlap between features of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD), it appears that cerebral hypoperfusion is the common underlying pathophysiological mechanism which is a major contributor to cognitive decline and degenerative processes leading to dementia. Sustained cerebral hypoperfusion is suggested to be the cause of white matter attenuation, a key feature common to both AD and dementia associated with cerebral small vessel disease (SVD). White matter changes increase the risk for stroke, dementia and disability. A major gap has been the lack of mechanistic insights into the evolution and progress of VCID. However, this gap is closing with the recent refinement of rodent models which replicate chronic cerebral hypoperfusion. In this review, we discuss the relevance and advantages of these models in elucidating the pathogenesis of VCID and explore the interplay between hypoperfusion and the deposition of amyloid β (Aβ) protein, as it relates to AD. We use examples of our recent investigations to illustrate the utility of the model in preclinical testing of candidate drugs and lifestyle factors. We propose that the use of such models is necessary for tackling the urgently needed translational gap from preclinical models to clinical treatments.

Cortical microinfarcts (CMIs) observed in brains of patients with Alzheimer’s disease tend to be located close to vessels afflicted with cerebral amyloid angiopathy (CAA). CMIs in Alzheimer’s disease are preferentially distributed in the arterial borderzone, an area most vulnerable to hypoperfusion. However, the causal association between CAA and CMIs remains to be elucidated. This study consists of two parts: (1) an observational study using postmortem human brains (n = 31) to determine the association between CAA and CMIs, and (2) an experimental study to determine whether hypoperfusion worsens CAA and induces CMIs in a CAA mouse model. In postmortem human brains, the density of CMIs was 0.113/cm2 in mild, 0.584/cm2 in moderate, and 4.370/cm2 in severe CAA groups with a positive linear correlation (r = 0.6736, p < 0.0001). Multivariate analysis revealed that, among seven variables (age, disease, senile plaques, neurofibrillary tangles, CAA, atherosclerosis and white matter damage), only the severity of CAA was a significant multivariate predictor of CMIs (p = 0.0022). Consistent with the data from human brains, CAA model mice following chronic cerebral hypoperfusion due to bilateral common carotid artery stenosis induced with 0.18-mm diameter microcoils showed accelerated deposition of leptomeningeal amyloid β (Aβ) with a subset of them developing microinfarcts. In contrast, the CAA mice without hypoperfusion exhibited very few leptomeningeal Aβ depositions and no microinfarcts by 32 weeks of age. Following 12 weeks of hypoperfusion, cerebral blood flow decreased by 26% in CAA mice and by 15% in wild-type mice, suggesting impaired microvascular function due to perivascular Aβ accumulation after hypoperfusion. Our results suggest that cerebral hypoperfusion accelerates CAA, and thus promotes CMIs.Electronic supplementary materialThe online version of this article (doi:10.1007/s00401-011-0925-9) contains supplementary material, which is available to authorized users.

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Me, myself, and dye: Core‐unsubstituted perylene bisimide dyes bearing a melamine hydrogen‐bonding unit link with cyanurates giving H‐ (red, see picture) and J‐aggregates (green). In solution the aggregates can interconvert on thermal treatment or by changing the stoichiometry. In solid films the green to red color change occurs upon scratching the surface.