Alzheimer's disease with cerebrovascular disease: current status in the Asia-Pacific region.

BACKGROUND: There is growing awareness of the coexistence of Alzheimer's disease and cerebrovascular disease (AD+CVD), however, due to lack of well-defined criteria and treatment guidelines AD+CVD may be underdiagnosed in Asia. METHODS: Sixteen dementia specialists from nine Asia Pacific countries completed a survey in September 2014 and met in November 2014 to review the epidemiology, diagnosis and treatment of AD+CVD in Asia. A consensus was reached by discussion, with evidence provided by published studies when available. RESULTS: AD accounts for up to 60% and AD+CVD accounts for 10-20% of all dementia cases in Asia. The reasons for underdiagnosis of AD+CVD include lack of awareness as a result of a lack of diagnostic criteria, misdiagnosis as vascular dementia or AD, lack of diagnostic facilities, resource constraints and cost of investigations. There is variability in the tools used to diagnose AD+CVD in clinical practice. Diagnosis of AD+CVD should be performed in a stepwise manner of clinical evaluation followed by neuroimaging. Dementia patients should be assessed for cognition, behavioural and psychological symptoms, functional staging and instrumental activities of daily living. Neuroimaging should be performed using computed tomography or magnetic resonance imaging. The treatment goals are to stabilize or slow progression as well as to reduce behavioural and psychological symptoms, improve quality of life and reduce disease burden. First-line therapy is usually an acetylcholinesterase inhibitor such as donepezil. CONCLUSION: AD+CVD is likely to be under-recognised in Asia. Further research is needed to establish the true prevalence of this treatable and potentially preventable disease.

Experimental striatal degeneration induced by kainic acid administration: relevance to morphological changes in Huntington's disease.

In an attempt to reproduce the characteristic neuronal degeneration pattern in the striatum of human patients with Huntington's disease, the histological and ultrastructural features of the degeneration of medium-sized nerve cells in the striatum and its processes are described in young rats induced by a direct injection of a small amount of kainic acid into the striatum. A light microscopic examination revealed initial edema and necrotic changes at the site of injection. The area surrounding the needle track showed neuronal and dendritic swelling and eosinophilic neurons without the apparent involvement of the passing axons. Later changes consisted of a marked neuronal loss particularly of the small cells with consequent severe astrocytosis. Electron microscopy showed specific neuronal alterations in the form of ballooned Golgi apparatuses, swelling of the endoplasmic reticulum, dendritic swelling, proliferated neurofilaments and aggregation of polysomes together with a marked disruption of neuropil. Neuronal debris and small dense bodies appeared. The majority of neuronal loss consisted of medium-sized nerve cells: Type I. Some spheroid bodies and lipid droplets were also observed.

An ultrastructural study of Pick bodies.

We report the results of an ultrastructural study of Pick bodies (PB). A histogram constructed with the maximal width of each filamentous component in PB revealed a wide range of sizes among the filaments, in contrast to the unique composition of the paired helical filaments (PHF) seen in the neurofibrillary tangle of Alzheimer type (NFT-AT). Morphologically, three groups of filaments could be distinguished. The first group consisted of straight smooth-surfaced filaments of 10-14 nm diameter, which were presumably altered neurofilaments. The second one was of straight smooth-surfaced "tubules" of 15-22 nm diameter, smaller than normal microtubules. The third one was of PHF thought to be formed by a pair of filaments of the first group. The PHF found in PB differed from PHF of NFT-AT in the distance between crossovers, and rather resembled the loosely interwinding PHF reported in NFT of progressive supranuclear palsy.