Basic Science and Pathogenesis.

Background: Recent studies highlight distinct patterns of cortical atrophy between amnestic (typical) and non-amnestic (atypical, with subtypes: behavioural, dysexecutive, logopenic and visuospatial) clinical phenotypes of Alzheimer's disease (AD). The current study aimed to assess regional MRI patterns of cortical atrophy across AD phenotypes, and their association with amyloid-beta (Aβ), phosphorylated tau (pTau), axonal degeneration (NfL) and microvascular deterioration (COLIV).

Method: Postmortem In-situ 3DT1 3T-MRI data was collected for 33 AD (17 typical, 16 atypical) and 16 control brain donors.

Basic Science and Pathogenesis.

Background: The hippocampus is highly vulnerable to amyloid-b (Aβ) and phosphorylated tau (p-tau), and shows synaptic loss in Alzheimer's disease (AD). Moreover, the loss of synapses correlates strongly with cognitive decline and leads to neuronal network dysfunction. Here, we aim to map the selective synaptic loss in hippocampal and parahippocampal subregions in AD and its association to the severity of neuropathology, axonal damage and cognitive decline.

Evolutionary origins and functional diversification of Auxin Response Factors.

The Auxin Response Factors (ARFs) family of transcription factors are the central mediators of auxin-triggered transcriptional regulation. Functionally different classes of extant ARFs operate as antagonistic auxin-dependent and -independent regulators. While part of the evolutionary trajectory to the present auxin response functions has been reconstructed, it is unclear how ARFs emerged, and how early diversification led to functionally different proteins.

Alzheimer's disease clinical variants show distinct neuroinflammatory profiles with neuropathology.

Aims: Although the neuroanatomical distribution of tau and amyloid-β is well studied in Alzheimer's disease (AD) (non)-amnestic clinical variants, that of neuroinflammation remains unexplored. We investigate the neuroanatomical distribution of activated myeloid cells, astrocytes, and complement alongside amyloid-β and phosphorylated tau in a clinically well-defined prospectively collected AD cohort.

Methods: Clinical variants were diagnosed antemortem, and brain tissue was collected post-mortem.

The neocortical infrastructure for language involves region-specific patterns of laminar gene expression.

The language network of the human brain has core components in the inferior frontal cortex and superior/middle temporal cortex, with left-hemisphere dominance in most people. Functional specialization and interconnectivity of these neocortical regions is likely to be reflected in their molecular and cellular profiles. Excitatory connections between cortical regions arise and innervate according to layer-specific patterns.