-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
At present, the most widely accepted pathogenesis of AD is the amyloid cascade hypothesis, which believes that AD is mainly caused by the accumulation of β-amyloid (Aβ) peptides in senile plaques, followed by the accumulation of misfolded tau protein in senile plaques.
Results, neuronal loss, cognitive decline, and loss of independence in activities of daily living (ADL)
.
An expected result of the amyloid cascade hypothesis is that regulating the production of Aβ levels in the brain should prevent the downstream effects of this pathology, thereby slowing the progression of the disease
.
Therefore, in the field of AD research, resolving the divergence between the overwhelming evidence of amyloid as a disease driver and the failure of most (but not all) anti-amyloid treatments is a major unresolved issue
.
Experimental studies have shown that the balance between short Aβ and long Aβ species may regulate the toxic effect of Aβ in Alzheimer's disease (AD), but clinical evidence is lacking
.
.
Nicholas Cullen et al.
studied whether Aβ38 levels in cerebrospinal fluid (CSF) are related to the risk of AD dementia and cognitive decline
Nicholas Cullen and others
The level of Aβ38 in cerebrospinal fluid of 656 individuals was measured in two clinical cohorts of the Swedish BioFINDER study and the Alzheimer's Neuroimaging Initiative (ADNI)
.
The Cox regression model is used to evaluate the baseline Aβ38 level of patients with positive AD biomarkers ( AD+; measured by the ratio of P-tau/Aβ42 in cerebrospinal fluid ) , subjective cognitive decline ( SCD) or mild cognitive impairment ( MCI) .
The relationship between AD dementia risk .
The Cox regression model is used to evaluate the baseline Aβ38 level of patients with positive AD biomarkers ( AD+; measured by the ratio of P-tau/Aβ42 in cerebrospinal fluid ) , subjective cognitive decline ( SCD) or mild cognitive impairment ( MCI) .
The distribution of cerebrospinal fluid Aβ38 levels in the diagnosis group and cohort and its correlation with cerebrospinal fluid Aβ42 and cerebrospinal fluid P-tau protein
Study on the correlation between cerebrospinal fluid Aβ38 and longitudinal cognition
In the BioFINDER cohort, high Aβ38 levels were associated with a slower decline in MMSE (β = 0.
30 points/standard deviation, P = 0.
001) and a lower risk of conversion to AD dementia (HR = 0.
83/standard deviation, P = 0.
03)
.
High Aβ38 levels are associated with a slower decline in MMSE (β = 0.
Higher levels of Aβ38 were associated with less reduction in MMSE (β = 0.
Study on the Correlation between Cerebrospinal Fluid Aβ38 and Clinical Transformation
In two independent clinical cohorts, higher CSF Aβ38 levels were associated with lower risk of AD-related changes
.
A higher CSF Aβ38 level is associated with a lower risk of AD-related changes
Original source
Cullen, Nicholas et al.
“Association of CSF Aβ38 Levels With Risk of Alzheimer Disease-Related Decline.
Leave a message here
