2026-01-08 14:52 |
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2026-01-08 14:50 |
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2026-01-08 14:47 |
[DZNE-2026-00043]
Abstract/Journal Article
He, B. ; Ospina, P. ; Espinosa, A. ; et al
Early changes in basal forebrain volume and cognitive function in preclinical autosomal dominant Alzheimer's disease
Background: The basal forebrain (BF), home to cholinergic neurons essential for attention and memory undergoes structural changes in sporadic Alzheimer's Disease and in at-risk individuals, contributing to cognitive decline. To investigate whether BF volume is reduced in preclinical autosomal-dominant Alzheimer's disease (ADAD), we studied cognitively-unimpaired carriers of the PSEN1 E280A mutation from the Colombian kindred, the largest ADAD cohort with a single mutation, known for early cognitive decline (mild cognitive impairment at age 44, dementia at 49). [...]
OpenAccess: PDF PDF (PDFA);
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2026-01-08 14:46 |
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2026-01-08 14:44 |
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2026-01-07 16:33 |
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2026-01-07 16:14 |
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2026-01-07 15:47 |
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2026-01-06 10:21 |
[DZNE-2026-00035]
Journal Article
Klassen, P. C. ; Alexudis, C. ; Klose, V. ; et al
Increased transmembrane protein 119 (TMEM119) levels in the cerebrospinal fluid of patients with mild cognitive impairment due to Alzheimer's disease suggest early microglial involvement.
We aimed to evaluate the potential of the microglial marker transmembrane protein 119 (TMEM119) in the cerebrospinal fluid (CSF) as a (differential) diagnostic biomarker for neurodegenerative diseases.Following assay validation, we used enzyme-linked immunosorbent assay to measure CSF TMEM119 in 174 patients from six diagnostic groups: Alzheimer's disease (AD, n = 35), amyotrophic lateral sclerosis (ALS, n = 33), cerebral microangiopathy (CM, n = 25), frontotemporal lobar degeneration (FTLD, n = 28), Lewy body diseases (n = 21), and non-neurodegenerative controls (n = 33).CSF TMEM119 levels were elevated in the AD group compared to the control (p = 0.004), CM (p = 0.005), and FTLD (p = 0.023) groups. Levels were higher in both mild cognitive impairment (MCI-AD) and dementia (ADD) subgroups when compared to controls. [...]
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2026-01-05 09:51 |
[DZNE-2026-00021]
Journal Article
Torre, E. ; Faure, M. ; Bidaud, I. ; et al
L-Type Cav1.3 and HCN Channels Mediate Heart Rate Acceleration by Catecholamines.
The ionic mechanism by which catecholamines increase the heart rate is incompletely understood. In this study, we have assessed the roles of sinoatrial node L-type Cav1.3 (α1D) Ca2+ channels, phosphorylation of L-type channel regulatory partner protein Rad (Ras-related RGK GTP-binding protein), and cAMP-dependent regulation of hyperpolarization-activated HCN (hyperpolarization-activated cyclic nucleotide-gated) channels.We studied β-adrenergic regulation of heart rate and sinoatrial pacemaker activity in mice lacking Cav1.3 channels and in mice expressing dihydropyridine-insensitive L-type Cav1.2 channels alone or concomitantly expressing cAMP-insensitive HCN4 subunits in a heart-specific and time-controlled manner. [...]
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