TGF-β1 factor in the cerebrovascular diseases of Alzheimer’s disease

Transforming growth factor betas (TGF-βs) belong to three isoforms (TGF-β1, TGF-β2 and TGF-β3) members of a large pleiotropic superfamily of around 100 distinct proteins participating in the regulation of key events of development and disease, and tissue repair. In the central nervous system (CNS), all the three isoforms are produced by both glial and neuronal cells and are involved in essential tissue functions such as cell-cycle control, regulation of early development and differentiation, neuronal survival and astrocytes differentiation. Recent findings have shown abnormally increase of the levels of TGF-β1 in the brain of patients suffering Alzheimer's disease (AD), an elderly pathology reaching individuals over 65-years-old which present well-known hallmarks, including cerebrovascular deficiency, abnormal deposition of amyloid beta (Aβ), cholinergic denervation, neuroinflammation, neurofibrillary tangles and progressive loss of memory. However, related to the pathological features of AD, the brain overexpression of TGF-β1 was associated with neuroinflammation, accumulation of extracellular matrix compounds and cerebrovascular stiffness, neuronal apoptosis along with the development of vascular hypertrophy. Consistent with these observations, transgenic mice model (TGF mice) overexpressing constitutively TGF-β1 fully mimicked AD-like cerebrovascular pathology. Taken altogether, these data suggest the involvement of TGF-β1in the pathogenesis of AD, particularly in the cerebrovascular pathology which is of interest in the present review that will discuss the contribution of TGF-β1 in the cerebrovascular physiopathology of AD.

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