The concentrations of selected metabolites in the hippocampus and cerebellum of 13 Alzheimer's diseased (AD) and four nondemented postmortem brains were measured using high resolution 1H NMR spectroscopy. For both the hippocampal region and the cerebellum, the putative neuronal marker N-acetyl aspartate (NAA) was significantly lower in AD brains relative to the nondemented brains. For the hippocampal region, the NAA concentration correlated inversely with semiquantitative assessments of neuronal loss and neurofibrillary tangles. The gamma-aminobutyric acid levels in both hippocampus and cerebellum of an age- and a postmortem interval-matched subset of AD brains were lower than those of the controls. Because the cerebellum is generally thought to be unaffected by AD, the NAA decrease in the Alzheimer cerebellum may be due to lesions of either the Alzheimer or non-Alzheimer type in contralateral cerebrum.
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http://dx.doi.org/10.1093/gerona/52a.2.b111 | DOI Listing |
Alzheimers Dement
December 2024
Department of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Adenosine receptor 1 (A1R) is the predominant subtype of adenosine receptors, primarily distributed in memory-associated brain regions such as the cortex, hippocampus, and cerebellum. It actively participates in plasticity-regulated synaptic transmission and is crucial for functions related to sleep, arousal, cognition, learning, and memory. In a recent study, we reported that an elevation in A1R signaling mediates aberrant neuron-glial crosstalk in Alzheimer's disease.
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December 2024
Texas A&M University, College Station, TX, USA.
Background: Older females, particularly susceptible to Alzheimer's disease (AD), may be affected by hormonal fluctuation during life. We aim to investigate the relationship between changes in brain volume and sex steroid hormones over time. We hypothesize that levels of sex hormones (17ß-estradiol, progesterone, and testosterone) relate to changes in brain volume, especially in the hippocampus (HPC) and cerebellum (CB).
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December 2024
Laboratory of Neuro Imaging, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Background: Mutations in the presenilin 1 (PSEN1) gene cause early onset autosomal dominant Alzheimer's Disease (AD), and the Jalisco mutation (A431E) is a subset found in people of Mexican descent (Yescas P, 2006). The Jalisco A431E mutation has been shown to produce distinct AD neuropathology such as cotton-wool amyloid plaques as well as motor dysfunction like spastic paraparesis (Orozco-Barajas, 2022). High levels of tau neuropathology have been observed with other PSEN1 mutations, but tau neuropathology in Jalisco patients has not been examined.
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December 2024
Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Background: Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) plaques and tau tangles in the brain, and neurotransmission dysfunctions. Indeed, our group recently demonstrated that the γ-aminobutyric acid (GABA)ergic system is vulnerable to AD pathology in humans. However, whether this vulnerability is also present in AD rodent models is still unknown.
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December 2024
Hospital del Mar Research Institute (IMIM), Barcelona, Spain.
Background: Objective Subtle Cognitive Decline (obj-SCD) can be identified through standardized neuropsychological tests and may precede the development of Mild Cognitive Impairment (MCI). Nevertheless, current clinical and research criteria lack a standardized protocol for identifying obj-SCD. This study introduces cutting-edge sensitive methods to characterize obj-SCD, defined through Alzheimer's disease (AD) biomarker-based longitudinal cognitive performance in episodic memory.
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