The accuracy of computed tomography, electroencephalography, and clinical features in the differential diagnosis of senile dementia was studied prospectively. Out of 50 demented patients, autopsy revealed 32 cases with either senile dementia of the Alzheimer's type (SDAT), multi-infarct dementia (MID), or a combination of both. Eighteen patients had dementia caused by other diseases. Based on a combination of computed tomography, electroencephalography, and clinical features, senile dementia of the Alzheimer's type was differentiated from all 50 patients, with a specificity of 83% and a sensitivity of 80%. Focusing on senile dementia of the Alzheimer's type, multi-infarct dementia, or a combination of both, specificity decreased to 65% and sensitivity to 47%. Comparing the different methods, multi-infarct processes were diagnosed with a higher sensitivity by the clinical features (73%) than by computed tomography (18%) or electroencephalography (18%). None of the methods validly differentiated multi-infarct dementia from a combination of multi-infarct dementia and senile dementia of the Alzheimer's type.
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http://dx.doi.org/10.1001/archneur.1989.00520470081031 | DOI Listing |
Clin EEG Neurosci
January 2025
Palma Sola Neurology Associates, Bradenton, FL, USA.
Evoked potential metrics extracted from an EEG exam can provide novel sources of information regarding brain function. While the P300 occurring around 300 ms post-stimulus has been extensively investigated in relation to mild cognitive impairment (MCI), with decreased amplitude and increased latency, the P200 response has not, particularly in an oddball-stimulus paradigm. This study compares the auditory P200 amplitudes between MCI (28 patients aged 74(8)) and non-MCI, (35 aged 72(4)).
View Article and Find Full Text PDFProteomics
January 2025
Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Alzheimer's disease (AD) is a leading cause of dementia, but the pathogenesis mechanism is still elusive. Advances in proteomics have uncovered key molecular mechanisms underlying AD, revealing a complex network of dysregulated pathways, including amyloid metabolism, tau pathology, apolipoprotein E (APOE), protein degradation, neuroinflammation, RNA splicing, metabolic dysregulation, and cognitive resilience. This review examines recent proteomic findings from AD brain tissues and biological fluids, highlighting potential biomarkers and therapeutic targets.
View Article and Find Full Text PDFJ Alzheimers Dis
January 2025
Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China.
Background: Plasma biomarkers demonstrated potential in identifying amyloid pathology in early Alzheimer's disease. Different subtypes of subjective cognitive decline (SCD) may lead to different cognitive impairment conversion risks.
Objective: To investigate the differences of plasma biomarkers in SCD subtypes individuals, which were unclear.
J Alzheimers Dis
January 2025
Alzheimer Centrum Limburg, Mental Health and Neuroscience Research Institute (MHeNs), Department of Psychiatry and Neuropsychology, Maastricht University, Maastricht, Netherlands.
Background: There is consistent evidence for the contribution of modifiable risk factors to dementia risk, offering opportunities for primary prevention. Yet, most individuals are unaware of these opportunities.
Objective: To investigate whether online education about dementia risk reduction may be a low-level means to increase knowledge and support self-management of modifiable dementia risk factors.
J Alzheimers Dis
January 2025
Department of Gerontology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Background: Urinary formic acid (FA) has been reported to be a biomarker for Alzheimer's disease (AD). However, the association between FA and pathological changes in memory clinic patients is currently unclear.
Objective: This study aims to investigate associations between FA and pathological changes across different cognitive statuses in memory clinic patients.
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