The human 'P1' middle latency evoked potential is postulated to be generated in the thalamus by a cholinergic component of the ascending reticular activating system. To test the hypothesis that P1 and its generator substrate are abnormal in Alzheimer's disease (AD), a disorder of marked cholinergic deficiency, recordings of middle latency responses to click stimuli were carried out. Comparisons between the AD and age-matched control groups indicated normal auditory brain-stem and Pa responses but a significant decrease in P1 amplitude. This P1 abnormality suggests that the midbrain cholinergic cells in AD may be dysfunctional.

Download full-text PDF

Source
http://dx.doi.org/10.1016/0168-5597(89)90005-1DOI Listing

Publication Analysis

Top Keywords

alzheimer's disease
8
middle latency
8
midlatency auditory
4
auditory evoked
4
evoked responses
4
responses differential
4
differential abnormality
4
abnormality alzheimer's
4
disease human
4
human 'p1'
4

Similar Publications

Over recent years, the retina has been increasingly investigated as a potential biomarker for dementia. A number of studies have looked at the effect of Alzheimer's disease (AD) pathology on the retina and the associations of AD with visual deficits. However, while OCT-A has been explored as a biomarker of cerebral small vessel disease (cSVD), studies identifying the specific retinal changes and mechanisms associated with cSVD are lacking.

View Article and Find Full Text PDF

Lewy body diseases and the gut.

Mol Neurodegener

January 2025

Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, 20815, USA.

Gastrointestinal (GI) involvement in Lewy body diseases (LBDs) has been observed since the initial descriptions of patients by James Parkinson. Recent experimental and human observational studies raise the possibility that pathogenic alpha-synuclein (⍺-syn) might develop in the GI tract and subsequently spread to susceptible brain regions. The cellular and mechanistic origins of ⍺-syn propagation in disease are under intense investigation.

View Article and Find Full Text PDF

The ApoE ε4 allele (APOEε4) is a major genetic risk factor for sporadic Alzheimer's disease (AD) and is linked to demyelination and cognitive decline. However, its effects on the lipid transporters apolipoprotein E (ApoE) and fatty acid-binding protein 7 (Fabp7), which are crucial for the maintenance of myelin in white matter (WM) during the progression of AD remain underexplored. To evaluate the effects of APOEε4 on ApoE, Fabp7 and myelin in the WM of the frontal cortex (FC), we examined individuals carrying one ε4 allele that came to autopsy with a premortem clinical diagnosis of no cognitive impairment (NCI), mild cognitive impairment (MCI) and mild to moderate AD compared with non-carrier counterparts.

View Article and Find Full Text PDF

Previous studies have suggested that systemic viral infections may increase risks of dementia. Whether this holds true for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus infections is unknown. Determining this is important for anticipating the potential future incidence of dementia.

View Article and Find Full Text PDF

Toward a biological definition of neuronal and glial synucleinopathies.

Nat Med

January 2025

Department of Neurology & Neurological Sciences, Stanford Movement Disorders Center, Stanford University, Stanford, CA, USA.

Cerebral accumulation of alpha-synuclein (αSyn) aggregates is the hallmark event in a group of neurodegenerative diseases-collectively called synucleinopathies-which include Parkinson's disease, dementia with Lewy bodies and multiple system atrophy. Currently, these are diagnosed by their clinical symptoms and definitively confirmed postmortem by the presence of αSyn deposits in the brain. Here, we summarize the drawbacks of the current clinical definition of synucleinopathies and outline the rationale for moving toward an earlier, biology-anchored definition of these disorders, with or without the presence of clinical symptoms.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!