Publications by authors named "A Haapasalo"
Article Synopsis
- In Alzheimer's disease, amyloid beta (Aβ) triggers the cleavage of the TrkB-FL receptor, disrupting essential BDNF signaling that is crucial for neuron health and function.
- Researchers found that TrkB-FL cleavage occurs early in the disease and worsens with increased pathology, using human samples and cerebrospinal fluid for their studies.
- They developed a TAT-TrkB peptide that successfully prevents TrkB-FL cleavage, showing potential in improving cognitive function and synaptic issues in a mouse model of Alzheimer's, indicating it could be a safe and effective treatment option.
Article Synopsis
- - The study examines the incidence and prevalence of early-onset dementia (EOD) in two areas of Finland from 2010 to 2021, finding that the crude incidence rate was 12.3 cases per 100,000 persons per year with specific age groups showing higher rates.
- - Out of the 794 new EOD cases identified, Alzheimer’s disease (AD) was the most common subtype, making up 48.2% of cases, followed by behavioral variant frontotemporal dementia at 12.7%.
- - The findings indicate that the incidence rates for EOD are higher than previous reports, with a notable increase in early-onset AD cases over time, while other EOD subtypes remained
We investigated the effects of daily ultraviolet A1 (UV-A1, 340-400 nm) exposures on mood states (#R19055, approval on 21 October 2020). Based on our earlier findings of the influence of diurnal preference on mood, we investigated further whether diurnal preference plays a role in the influence of UV-A1 on mood states. Forty-one healthy participants aged 19-55 years were randomized to receive either UV-A1 (n = 21) or control (n = 20) exposures (violet light, 390-440 nm).
View Article and Find Full Text PDFAutoantibodies directed against the GluA3 subunit (anti-GluA3 hIgGs) of AMPA receptors have been identified in 20%-25% of patients with frontotemporal lobar degeneration (FTLD). Data from patients and in vitro/ex vivo pre-clinical studies indicate that anti-GluA3 hIgGs negatively affect glutamatergic neurotransmission. However, whether and how the chronic presence of anti-GluA3 hIgGs triggers synaptic dysfunctions and the appearance of FTLD-related neuropathological and behavioural signature has not been clarified yet.
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