Lower amygdala and hippocampal volume correlates with TDP‐43 load in limbic‐predominant age‐related TDP‐43 encephalopathy (LATE).

Background: Limbic‐predominant age‐related TDP‐43 encephalopathy (LATE) is often described as occurring in older individuals, either with or without co‐occurring neurodegenerative disease. Because the presence of LATE can only be determined post mortem, little is known about the clinical and neuroimaging features of LATE. The current study aims to assess the correlation between LATE and MRI‐measured amygdala and hippocampal volume in Alzheimer’s disease (AD) and Lewy Body Diseases (LBD), including Parkinson’s disease (PD), PD dementia, and dementia with Lewy Bodies

Methods: Post‐mortem in‐situ 3DT1 3T‐MRI data were collected for 51 cases (27 AD and 24 LBD) of which 17 had post‐mortem confirmed LATE neuropathological change (9 AD and 8 LBD), as well as 34 non‐LATE (18 AD and 16 PD) donors (matched on age, sex, and Braak stage).

Lower amygdala and hippocampal volume correlates with TDP‐43 load in limbic‐predominant age‐related TDP‐43 encephalopathy (LATE).

Background: Limbic‐predominant age‐related TDP‐43 encephalopathy (LATE) is often described as occurring in older individuals, either with or without co‐occurring neurodegenerative disease. Because the presence of LATE can only be determined post mortem, little is known about the clinical and neuroimaging features of LATE. The current study aims to assess the correlation between LATE and MRI‐measured amygdala and hippocampal volume in Alzheimer’s disease (AD) and Lewy Body Diseases (LBD), including Parkinson’s disease (PD), PD dementia, and dementia with Lewy Bodies

Methods: Post‐mortem in‐situ 3DT1 3T‐MRI data were collected for 51 cases (27 AD and 24 LBD) of which 17 had post‐mortem confirmed LATE neuropathological change (9 AD and 8 LBD), as well as 34 non‐LATE (18 AD and 16 PD) donors (matched on age, sex, and Braak stage).

Distinct tau and alpha-synuclein molecular signatures in Alzheimer's disease with and without Lewy bodies and Parkinson's disease with dementia.

Alpha-synuclein (aSyn) pathology is present in approximately 50% of Alzheimer's disease (AD) cases at autopsy and might impact the age-of-onset and disease progression in AD. Here, we aimed to determine whether tau and aSyn profiles differ between AD cases with Lewy bodies (AD-LB), pure AD and Parkinson's disease with dementia (PDD) cases using epitope-, post-translational modification- (PTM) and isoform-specific tau and aSyn antibody panels spanning from the N- to C-terminus. We included the middle temporal gyrus (MTG) and amygdala (AMY) of clinically diagnosed and pathologically confirmed cases and performed dot blotting, western blotting and immunohistochemistry combined with quantitative and morphological analyses.

Reactive astrocytes as treatment targets in Alzheimer's disease-Systematic review of studies using the APPswePS1dE9 mouse model.

Astrocytes regulate synaptic communication and are essential for proper brain functioning. In Alzheimer's disease (AD) astrocytes become reactive, which is characterized by an increased expression of intermediate filament proteins and cellular hypertrophy. Reactive astrocytes are found in close association with amyloid-beta (Aβ) deposits.