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Although ideomotor limb apraxia is considered to be a typical sign of cortical pathologies such as Alzheimer’s disease (AD), it has been also reported in subcortical neurodegenerative diseases and vascular lesions. We aimed to investigate the difference between AD, subcortical vascular dementia (SVaD) and mild cognitive impairment (MCI) patients by means of ideomotor limb apraxia frequency and severity. Ninety-six AD, 72 SVaD, and 84 MCI patients were assessed with the mini-mental status examination (MMSe), clinical dementia rating (CDR) and the apraxia screening test of TULIA (AST). Apraxia was significantly more frequent in the AD patients (32.3%) than in both of the SVaD (16.7%) and MCI (4.8%) patients. The frequency of apraxia was also significantly higher in SVaD patients than in MCI patients. AD patients had significantly lower apraxia scores than both SVaD and MCI patients. In addition, a significant difference was found between SVaD and MCI patients in terms of apraxia scores. These results suggest that the widespread belief of the association between apraxia and cortical dementias is not exactly correct. The significant difference between both of the dementia groups and the MCI patients suggests that the absence of apraxia can be an indicator for MCI diagnosis.

ObjectiveThis study was performed to assess the efficacy of memantine in patients with amnestic mild cognitive impairment (aMCI).MethodsThirty healthy controls and 45 patients diagnosed with aMCI based on the Petersen criteria were classified into 3 groups. Group 1 comprised patients who received a single memantine dose following examination (n = 25), Group 2 comprised patients who did not receive memantine treatment following examination (n = 20), and Group 3 comprised healthy age-matched volunteers (n = 30). Neuropsychological testing was performed, and the response to memantine was examined at baseline and at 12, 24, and 48 weeks. Single-photon emission computed tomography was performed at baseline and at 48 weeks in patients who received memantine treatment.ResultsMemantine treatment significantly improved the symptoms of aMCI according to the Wechsler Adult Intelligence Scale-Revised vocabulary subtest, backward digit span, and Blessed Dementia Rating Scale, all of which were recorded for the duration of the study.ConclusionThese data indicate that patients with aMCI receiving memantine develop an improved semantic memory compared with no treatment. Further studies including larger patient cohorts are necessary to validate these findings.

Alzheimer's disease is an age-related progressive neurodegenerative disorder. The two major neuropathologic hallmarks of Alzheimer's disease (AD) are extracellular Amyloid beta (Aβ) plaques and intracellular neurofibrillary tangles (NFTs). A number of additional pathogenic mechanisms, possibly overlapping with Aβ plaques and NFTs formation, have been described, including inflammation, oxidative damage, iron dysregulation, cholesterol metabolism. To date, only symptomatic treatments exist for this disease, all trying to counterbalance the neurotransmitter disturbance. To block the progression of the disease they have to interfere with the pathogenic steps responsible for the clinical symptoms, including the deposition of extracellular amyloid β plaques and intracellular neurofibrillary tangle formation, inflammation and stem cell. In this review, we discuss new potential disease-modifying therapies for AD that are currently being studied in phase I-III trials.

Variant Creutzfeldt-Jakob disease (vCJD) was first reported in the UK in 1996. Here, we report the first Turkish case of vCJD. A 47-year-old man, who has never lived outside of Turkey and had had no transfusion, was admitted to the University Hospital with speech disorder, cognitive decline and ataxia following depression, irritability, and personality change. The immunoassay of the 14-3-3 protein in the cerebrospinal fluid was negative. Brain magnetic resonance imaging revealed high-signal lesions involving the bilateral caudate and lentiform nucleus on T₂- and diffusion-weighted imaging. The patient developed akinetic mutism 10 months after disease onset. The clinical presentation and neuroimaging findings were compatible with the vCJD cases reported since 1996 and met the World Health Organization’s case definition for probable vCJD.