Presubiculum principal cells are preserved from degeneration in knock-in APP/TAU mouse models of Alzheimer’s disease

Impaired long-range excitatory time scale predicts abnormal neural oscillations and cognitive deficits in Alzheimer’s disease

“…This result is also in concordance with a recent study demonstrating long-range axonal connectivity disruption in AD transgenic mice [40]. Increased pyramidal neuron time constants have also been reported in AD mouse models [41].…”

The fate of interneurons, GABAA receptor sub‐types and perineuronal nets in Alzheimer's disease

“…In contrast to PV‐expressing interneurons, have shown using a second‐generation knock‐in APP mouse model, that CR interneurons in AD are preserved anatomically and functionally, despite the presence of post‐phenotypic alterations, that is, the presence of neuroinflammation and pathological Aβ protein aggregation [ 39 ]. This specific resilience is not just limited to cells, in fact some regions like the presubiculum, also show unique ‘preserved’ morphology with an intact functional profile [ 40 , 41 ].…”

The relationships between neuroglial alterations and neuronal changes in Alzheimer’s disease, and the related controversies I: Gliopathogenesis and glioprotection

“…Different morphologies have also been described in other areas of these brains. The forms with extensions also invade some subtypes of amyloid plaques and the round forms are close the plaques as well diffusely distributed in the brain parenchyma (Figures 12,13,and 14). Different microglial phenotypes have been described, 127,130,138,140,141,158,160 but no clear microglial responses have been associated to specific alterations in specific areas of the brain or in specific phases of the progression of AD A decrease in ramified (considered healthy) microglia was recently described in subjects with advanced AD, 130 with imaging analysis demonstrating a reduction in the arborized area and skeletal complexity.…”

“…have been used to study neurons in normal and pathological situations, both in "healthy" and "Alzheimer" individuals, as well as in experimental models of AD. [8][9][10][11][12][13][14][15][16][17][18] In most human studies and in many pathogenic models of AD, was considered that glial cells also "suffer concomitant alterations", and these alterations are thought to aggravate neurodegeneration, [19][20][21][22][23][24][25][26][27][28][29][30][31][32] representing key changes in the pathogenic cascades that provoke neurodegeneration/dementia. However, the specific study of glial cells in AD begins many decades after (except for exceptions that are later mentioned).…”