Neurovascular unit
The neurovascular unit (NVU) comprises the components of the brain that collectively regulate cerebral blood flow in order to deliver the requisite nutrients to activated neurons.
Since 2001, though, the rapid increase of scientific papers citing the neurovascular unit represents the growing understanding of the interactions that occur between the brain’s cells and blood vessels.
[3] This mechanism controls oxygen and nutrient levels using vasodilation and vasoconstriction in a multidimensional process involving the many cells of the neurovascular unit, along with multiple signaling molecules.
[6] Thus, the NVU provides the architecture behind neurovascular coupling, which connects neuronal activity to cerebral blood flow and highlights the interdependence of their development, structure, and function.
Neuroimaging techniques that directly or indirectly monitor blood flow, such as fMRI and PET scans, can, thus, measure and locate activity in the brain with precision.
Difficulties arise when angiotensin proteins are present in higher concentrations, as there is an associated increase in blood flow that leads to hypertension and potential disorders.
Various other types of neuroimaging also allow the NVU itself to be studied by providing visual insights into the complex interactions between neurons, glial cells, and blood vessels in the brain.
[19] Fluorescence imaging offers excellent spatial resolution, allowing for detailed visualization of cellular morphology and localized molecular interactions.
Transmission electron microscopy images thin tissue sections, providing detailed information about the fine cellular structures, including synapses and organelles.
[23] However, it requires sample preparation involving fixation, dehydration, and staining, which can introduce artifacts, and it is not suitable for live or large-scale imaging due to its time-consuming nature.
It has limited temporal resolution, though, and its ability to visualize finer cellular and molecular details within the neurovascular unit is relatively lower compared to microscopy techniques.
[28] In particular, neurovascular failure can be caused by problems arising in the blood vessels, including blockages (embolism), clot formation (thrombosis), narrowing (stenosis), and rupture (hemorrhage).
[29] Ultimately, vascular dysfunction results in decreased cerebral blood flow and abnormalities in the blood–brain barrier, which poses a threat to the normal functioning of the brain.
[29][33] The breakdown of neurovascular coupling (e.g., modulations in neuronal activity that cause changes in local blood flow[8]) and the pathophysiology of the NVU is commonly observed across a wide variety of neurological and psychiatric disorders, including Alzheimer’s disease.
[29] The combination of recent hypotheses and evidence suggests that the pathophysiology of the NVU may contribute to cognitive impairment and be an initiating trigger for neurological manifestations of diseases such as Alzheimer's and dementia.
Destruction of the organization of the blood–brain barrier, decreased cerebral blood flow, and the establishment of an inflammatory context often result in neuronal damage since these factors promote the aggregation of β-amyloid peptide in the brain.
[37] During a review of various consortium data, it was shown that more than 30% of AD cases exhibit cerebrovascular disease on post-mortem examination, and almost all have evidence of cerebral amyloid angiopathy, microvascular degeneration, and white matter lesions.
[40] Common features of Huntington's include involuntary movements (chorea), bradykinesia, psychiatric symptoms, and cognitive decline, all of which are accelerated through neuronal cell death.
[41][42] The idea that neurovascular impairments may contribute to early neuronal cell loss in Huntington’s disease has been attracting significant attention in the HD community.
[46] It has also been proposed that neurovascular dysregulation manifests earlier in Huntington's than other pathologies, triggering innate immune signaling and a reduction of protein levels critical for maintaining the blood–brain barrier.
