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Cerebral amyloid angiopathy (CAA) is a degenerative neurovascular disease in which the protein amyloid-beta accumulates in the vessel wall of cortical and leptomeningeal arteries. This may lead to acute lobar cerebral haemorrhage, which in case of CAA is fatal in 10-30% of cases. CAA may also present with transient focal neurological episodes (TFNE), the symptoms of which may mimic a transient ischaemic attack (TIA). Distinction between the two has important implications for therapy, as antithrombotics are relatively contra-indicated in CAA, but indicated after a TIA. We describe a patient with transient focal neurological deficits who was initially treated with antithrombotic therapy for a suspected TIA. Eventually, the diagnosis CAA was made and antithrombotic treatment was ceased. This case stresses the importance of considering the diagnosis CAA with TFNE in patients presenting with transient neurological deficits, in order to avoid an unnecessarily increased risk of symptomatic and possibly fatal cerebral haemorrhage.

Until a few years ago, amyloid plaques in the brains of patients with Alzheimer's disease could only be demonstrated by means of neuropathological examination. New PET tracers allow for visualisation of these amyloid plaques in living patients. Biological validity and clinical relevance of this technique have been established. Expertise in interpretation of the images and the diagnostic impact is required. Cost effectiveness and added value over existing methods in terms of diagnosis and prognosis are still being investigated.

An increasing number of people with mild cognitive impairment (MCI) visits a memory clinic to find out whether their symptoms indicate Alzheimer's disease (AD). Markers in cerebrospinal fluid are increasingly used for the diagnosis of Alzheimer's disease. In the short term, CSF biomarkers are more accurate in ruling out progression to AD-type dementia than demonstrating progression. The predictive value of the CSF biomarkers increases with longer-duration follow-up and declines with age. The added value of CSF biomarkers is not yet clear in MCI patients in whom extensive clinical, neuropsychological examination or imaging have already been performed.

Biomarkers in cerebrospinal fluid (CSF) are being used increasingly to diagnose early Alzheimer's disease (AD). A CSF profile that is suggestive of ad is an abnormal ratio of the proteins Ab1-42 to total tau.To describe the prevalence and prognosis of a CSF profile in patients without dementia but with subjective memory problems and mild cognitive impairments (MCI) at a memory clinic.A multi-centre study.A European multi-centre study showed that a CSF AD profile was often present in patients with subjective complaints and patients with MCI . The CSF AD profile predicted a decline in cognition and daily functioning over a period of 3 years in patients with MCI. Patients with amnestic MCI and a CSF AD profile developed AD more often within this period than patients without this profile.CSF markers suggestive of ad are common in persons without dementia. It may be possible to use these markers for the prognosis of patients who have MCI .

Alzheimer's disease (AD) is neuropathologically characterized by the presence of senile plaques. The formation of these plaques is caused by the accumulation of amyloid-beta protein (Aβ), a process that begins decades before the onset of the first clinical symptoms. Senile plaques can be visualized by using positron emission tomography (PET) and the tracer 11C-PIB. Such 'amyloid imaging' can contribute significantly to both early and differential diagnosis of Alzheimer's disease. In the future, amyloid imaging could also be useful for selecting patients for clinical trials and in evaluating the effects of disease modifying agents tailored at lowering Aβ burden.

Although the sporadic form of Alzheimer's disease is the most common, rare familial variants exist. Approximately 50% of these cases are caused by a mutation in the presenilin genes. Mutations in presinilin genes give rise to Alzheimer's disease in a dominant pattern of inheritance with an early age of onset (60 years). Both presenilins (PS-1 and PS-2) are transmembrane proteins localized in the intracellular membranes of the endoplasmatic reticulum and Golgi apparatus. This suggests they play a role in transport or sorting of proteins in the cell. Different lines of evidence directly link presenilin to the formation of beta-amyloid, an important constituent of senile plaques. PS-1 has an essential function during development: mice lacking intact PS-1 are not viable. In addition, structural and functional homologies have been identified between presenilins and Notch signal transduction pathways, which play a role in development. The discovery of the presenilin mutations has provided a new angle to Alzheimer's disease research. Eventually, this will probably greatly contribute to knowledge of the pathogenesis of the disease and in time support the development of novel therapeutic strategies.

Senile plaques belong to the pathological hallmarks of the brains of patients with Alzheimer's disease. There is an increasing amount of evidence that the formation of senile plaques is accompanied by an acute phase reaction, involving the production of several inflammation-associated proteins and the activation of microglial cells. The products of these inflammatory reactions may contribute to the fibrillogenesis of the amyloid beta protein, the major constituent of senile plaques. Both fibrils of the amyloid beta protein and products of activated microglial cells may be neurotoxic, leading to neuronal degeneration and to clinical symptoms of dementia. Recent epidemiological findings have drawn attention to the possibility of therapy with anti-inflammatory agents. Although the results of these studies suggest a beneficial effect of such therapy, further study is warranted to gain more insight into the fundamental aspects of such treatment as well as to develop specific drugs that have little side-effects.