![Loading...](https://link.springer.com/static/c4a417b97a76cc2980e3c25e2271af3129e08bbe/images/pdf-preview/spacer.gif)
-
Article
Open AccessQuantification of SNAP-25 with mass spectrometry and Simoa: a method comparison in Alzheimer’s disease
Synaptic dysfunction and degeneration are central to Alzheimer’s disease (AD) and have been found to correlate strongly with cognitive decline. Thus, studying cerebrospinal fluid (CSF) biomarkers reflecting sy...
-
Article
Open AccessPredicting progression and cognitive decline in amyloid-positive patients with Alzheimer’s disease
In Alzheimer’s disease, amyloid- β (A β) peptides aggregate in the lowering CSF amyloid levels - a key pathological hallmark of the disease. However, lowered CSF amyloid levels may also be present in cognitively ...
-
Article
Open AccessPerspectives in fluid biomarkers in neurodegeneration from the 2019 biomarkers in neurodegenerative diseases course—a joint PhD student course at University College London and University of Gothenburg
Until relatively recently, a diagnosis of probable Alzheimer’s disease (AD) and other neurodegenerative disorders was principally based on clinical presentation, with post-mortem examination remaining a gold s...
-
Article
Open AccessA single dose of the γ-secretase inhibitor semagacestat alters the cerebrospinal fluid peptidome in humans
In Alzheimer’s disease, beta-amyloid peptides in the brain aggregate into toxic oligomers and plaques, a process which is associated with neuronal degeneration, memory loss, and cognitive decline. One therapeu...
-
Article
Open AccessNeurogranin and YKL-40: independent markers of synaptic degeneration and neuroinflammation in Alzheimer’s disease
Neuroinflammation and synaptic degeneration are major neuropathological hallmarks in Alzheimer’s disease (AD). Neurogranin and YKL-40 in cerebrospinal fluid (CSF) are newly discovered markers indicating synapt...
-
Article
Open AccessAPLP1 as a cerebrospinal fluid biomarker for γ-secretase modulator treatment
Alzheimer’s disease brains are characterized by extracellular plaques containing the aggregated amyloid β42 (Aβ42) peptide and intraneuronal tangles containing hyperphosphorylated tau. Aβ42 is produced by sequent...
-
Article
Open AccessCharacterization of the postsynaptic protein neurogranin in paired cerebrospinal fluid and plasma samples from Alzheimer’s disease patients and healthy controls
Synaptic dysfunction and degeneration are central events in Alzheimer’s disease (AD) pathophysiology that are thought to occur early in disease progression. Synaptic pathology may be studied by examining prote...
-
Article
Open Accessβ-site amyloid precursor protein-cleaving enzyme 1(BACE1) inhibitor treatment induces Aβ5-X peptides through alternative amyloid precursor protein cleavage
The β-secretase enzyme, β-site amyloid precursor protein-cleaving enzyme 1 (BACE1), cleaves amyloid precursor protein (APP) in the first step in β-amyloid (Aβ) peptide production. Thus, BACE1 is a key target f...
-
Article
Open AccessA novel Aβ isoform pattern in CSF reflects γ-secretase inhibition in Alzheimer disease
LY450139 (semagacestat) inhibits γ-secretase, a key enzyme for generation of amyloid β (Aβ), the peptide deposited in plaques in Alzheimer disease (AD). Previous data have shown that LY450139 lowers plasma Aβ,...