Human immunodeficiency virus type 1 (HIV1) is neurotropic. One of the morphological changes that is seen in patients with acquired immunodeficiency syndrome (AIDS) is cerebral atrophy affecting various structures including the neocortex. The cause of atrophy is not known. The total number of neocortical neurons was estimated in formalin fixed brains of 12 males with AIDS and 12 male controls matched for age and height. The mean number of neocortical neurons was 16.0 x 10(9) (coefficient of variation = 0.11) in the AIDS patients compared with 21.9 x 10(9) (coefficient of variation = 0.22) in the controls, a difference of approximately six billion (p < 0.005, 2-tailed). The global neuronal loss was 37%, and affected all four neocortical lobes. Ten patients did not have a history of central nervous system symptoms; two patients had a history of dementia. The number of neurons in the AIDS cases was not associated with dementia. AIDS is the first disease in which a global loss of neocortical neurons has been demonstrated using unbiased stereological methods. The loss of more than one third of the neurons may partly explain the cortical atrophy. Focal neuron loss has been reported by several authors, but none have been based on unbiased methods. In this group of AIDS patients the severe loss of neurons did not correspond to neurological deficits.
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http://dx.doi.org/10.1111/j.1699-0463.1995.tb01401.x | DOI Listing |
Alzheimers Dement
December 2024
Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Karolinska Institutet, Stockholm, Sweden.
Background: Detecting early stages of Alzheimer's disease (AD) remains a crucial yet complex challenge. While recent interest has surged in detecting biomarkers linked with the disease preclinical phase, a comprehensive understanding of the concomitant peripheral biological pathways before the potential disease onset is necessary. We aim to explore the associations between the 18F-MK6240 tau PET tracer with plasma inflammatory markers, other AT(X)N biomarkers and episodic memory.
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December 2024
Huashan Hospital, Fudan University, Shanghai, Shanghai, China.
Background: Synaptic loss is identified as a strong correlate of cognitive impairment in Alzheimer's disease (AD). Pathological tau can induce direct toxicity to synapse and spread trans-synaptically across connected neurons. Recent neuroimaging evidence revealed that tau pathology propagates along interconnected brain regions throughout macroscale brain networks.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Institute for Stroke and Dementia Research, Ludwig-Maximilians-Universität München, LMU München, Munich, Germany.
Background: In Alzheimer's disease, Aβ triggers tau spreading which drives neurodegeneration and cognitive decline. However, the mechanistic link between Aβ and tau remains unclear, which hinders therapeutic efforts to attenuate Aβ-related tau accumulation. Preclinical research could show that tau spreads across connected neurons in an activity-dependent manner, and Aβ was shown to trigger neuronal hyperactivity and hyperconnectivity.
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December 2024
Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Background: The in vivo amyloid-β (A) and tau (T) biomarkers have been validated against the respective neuropathological burden of amyloid-β plaques and neurofibrillary tangles. We aimed to assess the impact of mixed pathologies on the interpretation of AT biomarker system.
Method: A subset of 71 ADNI participants with available neuropathological data and ante-mortem cerebrospinal fluid (CSF) sampling was analyzed.
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