Cerebrovascular Rescue of Aging Brain
Relinca (TP7193, TP0233) in Dementia
TP7193 for CNS (‘Relinca’) is designed as delivery-optimized, disease-modifying drug to prevent or rescue cerebrovascular derangement in pre-dementia and dementia.
TP7193SL supports the trophism of neurovascular functionality via anti-senescence, assisted endothelial barrier and synaptic connectivity, induced cerebral hypotension while is β-Amyloid / Tau stabilizer. Fast-track clinical entry shall shorten the inertial lag-time of classic Rx drugs to afford an early POC in controlled clinical setting.
Alzheimer's Diseases, mixed
Cerebrovascular disease is a common comorbidity in patients with Alzheimer’s disease (AD). It contributes additively to the cognitive impairment and to lower the threshold for the development of dementia. Accumulating evidence suggests that dysfunction of the cerebral vasculature and AD neuropathology interact in multiple ways. Vascular processes even proceed AD neuropathology, implicating a causal role in the etiology of AD. In AD, the cerebral vasculature undergoes pronounced cellular, morphological and structural changes, which alters regulation of blood flow, vascular fluid dynamics and vessel integrity. Stiffening of central blood vessels lead to transmission of excessive pulsatile energy to the brain microvasculature, causing end-organ damage. Moreover, a dysregulated hemostasis and chronic vascular inflammation further impede vascular function, where its mediators interact synergistically. Changes of the cerebral vasculature are triggered and driven by systemic vascular abnormalities common in aging, aggravated by concomitant CV diseases.
Vascular Dementia & VCI
Vascular dementia is now recognized as the second most common form of dementia after AD, and there is increasing awareness that targeting vascular risk may help to prevent dementia, even of the Alzheimer type. Vascular cognitive impairment (VCI) refers to all forms of cognitive disorder associated with cerebrovascular disease, regardless of the specific mechanisms involved. It encompasses the full range of cognitive deficits from mild cognitive impairment to dementia. In principle, any of the multiple causes of clinical stroke can cause VCI. Recent work highlights a role of microinfarcts, microhemorrhages, strategic white matter tracts, loss of microstructural tissue integrity, and secondary neurodegeneration. Vascular brain injury results in loss of structural and functional connectivity, hence compromises the functional networks within the brain. VCI is common both after stroke and in stroke-free individuals presenting to dementia clinics, and vascular pathology frequently coexists with neurodegenerative pathology, resulting in mixed forms of mild cognitive impairment or dementia.