Wiseman et al. report that the rapid neurodegeneration observed in MSA is driven by toxic α-synuclein fibrils invading neuronal nuclei, leading to cell death. They propose redefining MSA as a neuronal nuclear and oligodendroglial α-synucleinopathy. https://t.co/3gtOb4ts88

Did you know that the SWDBB relies solely on charitable donations to fund our activities? We have a new Crowdfunding page: https://t.co/78HgJrhgS4 please do share it if you able to.

TSPO PET is used to measure inflammation in dementia, but its cellular basis is unclear. Using PET imaging and post-mortem brain tissue, Wijesinghe et al. show that microglia are the key immune cells driving TSPO PET signal changes. https://t.co/hDtbE5NjZr

Delighted to share our work, out today in @MDJ_Journal ! We highlight alpha-synuclein SAA positivity in PSP and CBS patient CSF samples. This may represent Lewy body co-pathology which can impact on clinical course (1/2) @PSPAssociation @MDC_IoN_UCL https://t.co/6hqrKSRI3w

Fantastic work by the brilliant @SidRamanan!

Nature research paper: Fibrin drives thromboinflammation and neuropathology in COVID-19

Professor Gillian Bates FRS is awarded the Royal Society's Ferrier Medal for her work in understanding the molecular basis of Huntington’s disease and consistently producing highly impactful findings which have moulded the course of this field. #RSMedals https://t.co/eS4hhzMY6C

MHRA #Lecanemab decision for the UK is imminent, and favourable, according to Telegraph leak - not a “wonder drug” but a very important step forward. A major investment in dementia services is needed not just to deliver this drug, but increase early accurate diagnosis for all

Mikhailenko et al. find limbic-predominant age-related TDP-43 encephalopathy (LATE-NC) in more than 50% of a population aged ≥85 years, and conclude that it is one of the most significant determinants of dementia in the general late-life aged population. https://t.co/34C57isUll

Our work on blood-based inflammation markers in FTLD is published! We found a pro-inflammatory cytokine profile in patients that is associated with central inflammation and worse survival outcomes. Huge thanks to all families, colleagues and funders! https://t.co/HLlcVJH5C8

FTDP-17 mutations P301L and P301T in MAPT give rise to novel tau filament folds. Individuals with mutations of P301 have distinct tauopathies. Great work: @MSchweighauser, @sy31802, Alexey Murzin. As always with @SjorsScheres. https://t.co/HZ2Q4uK493

Nick Fox making the case that excess brain volume loss associated with Lecanemab (or other effective mAB’s) is associated with the removal of “space-occupying” structures, as amyloid plaques occupy ~6-8% of the cortex in autopsy studies. #AAIC24

Lecanemab attenuates the rate of tau (PET) accumulation. #AAIC24

The median time interval between becoming Tau PET positive and developing dementia is ~7 years and no T+ participant remained dementia-free after 15 years.

Well this was unexpected! We found that TDP-43 forms heteromeric amyloid filaments with a second protein, annexin A11, in the neurodegenerative disease FTLD-TDP Type C. Read the preprint here: https://t.co/Y5IxwpxwG2

V interesting paper and thread on the transmissibility of beta amyloid in iatrogenic AD

Great collaboration on the Cambridge-Munich axis for research in PSP and CBD! Thanks to all co-authors for this great collaborative effort, to all participants whose time in research makes the real difference, and to our funders! @racingdementia @AlzResearchUK @CambridgeBRC

Great display of #aurora last night at Wicken fen, Cambridgeshire

Brain banking has always been enormously valuable for neuroscience research. Here is a new exciting publication using @LNDbrainbank tissue studying the genetics of #Pick's #Disease. https://t.co/SjRYFSjDto

Lewy body pathology is found in ~50% of both sporadic and familial Alzheimer's disease. Levin et al. showed that: 1. 0/26 of asymptomatic and 3/27 (11%) of symptomatic AD mutation carriers tested positive on an α-synuclein seed amplification assay (SAA) in cerebrospinal fluid.