Decreased clearance of Aβ from the brain is related to the pathogenesis of Alzheimer's disease (AD). Kallikrein‐related peptidase 7 (KLK7) is an astrocyte‐derived Aβ degrading enzyme that affects the amyloid pathology. Thus, astrocytes could be an effective cellular target for AD.

Increased TNF/TNFR1 signaling plays a detrimental role in Alzheimer's disease pathology and is associated with morphological alterations at the choroid plexus in patients and mice, and neuroinflammation. Blocking TNFR1 signaling prevents cognitive decline in Alzheimer's disease mouse models.

Determination of the amyloid‐β secondary structure distribution in blood plasma by an immuno‐IR‐sensor correlates with PET scanning and CSF markers in Alzheimer's disease (AD) patients, with potentials to be an accurate, simple, and minimally invasive biomarker for early AD detection.

Aβ_1–42 triggers translation of axonal mRNAs whose protein products form signaling complexes that transmit the presence of Aβ_1–42 from the cellular periphery back to the neuronal soma.

Astrocytes resume proliferation specifically at the vascular wall after brain injury. Genetic increase of astrocyte proliferation reduces monocyte invasion at the injury site, while lack of monocyte invasion promotes astrocyte proliferation and reduces the GFAP⁺ scar.

The adaptor protein APPL2 induces activation of RIP‐Cre neurons in the VMH, which enhances sympathetic outflow to sWAT, sWAT beiging and cold tolerance.

Synaptotrophic defects in mouse brains lacking amyloid precursor protein (APP) expression can be selectively rescued by the non‐amyloidogenic APPsα fragment, for which α7‐nAChRs may constitute a physiological receptor.

Environmental stimuli and voluntary exercise, known to ameliorate dementia rescue adult neurogenesis in transgenic mouse models by activating phagocytic microglia to reduce amyloid‐β seeding.

In animal and cellular models of Alzheimer disease (AD) and in fibroblasts from AD patients, APP‐C99 levels are increased in mitochondria‐associated endoplasmic reticulum membrane (ER‐MAM) regions, resulting in perturbed lipid homeostasis and mitochondrial dysfunction.