Taarho Research Hub - Taarho Neurodegeneration Research Hub

Alzheimer’s Disease

Beyond plaques and tangles: Alzheimer’s is more than beta-amyloid or tau deposition. These markers are expressions of deeper network collapse, synaptic dysfunction, and neurovascular imbalance.

Synaptic signaling disruption often precedes neuron loss, metabolic stress impairs energy utilization, and sleep-dependent clearance via the glymphatic system declines before diagnosis. Understanding these overlooked mechanisms allows interventions that target network resilience rather than downstream pathology.

Alzheimer’s is best understood as a network collapse under cumulative stress rather than isolated protein accumulation.

References

Vascular Dementia

Vascular Dementia arises from impaired cerebral blood flow — microinfarcts, chronic hypoperfusion, or endothelial dysfunction. Often coexisting with Alzheimer’s pathology, it magnifies cognitive decline.

Even subtle microvascular injury disrupts white matter tracts, executive function, and memory networks. Blood-brain barrier breakdown accelerates inflammation, highlighting the essential link between circulation and cognition.

Cognition is inseparable from circulation; vascular inefficiency reshapes mental function long before major stroke occurs.

References

Lewy Body Dementia

LBD is defined by alpha-synuclein aggregation, network instability, and perceptual fluctuations. Visual hallucinations and Parkinsonian symptoms reflect widespread cortical and subcortical involvement.

Neurotransmitter imbalances extend beyond dopamine to cholinergic and noradrenergic systems. Cognitive fluctuation is a marker of network desynchronization, while REM sleep disruption often precedes clinical symptoms.

LBD represents temporal network instability, where cognition and perception lose rhythmic coherence.

References

Frontotemporal Dementia

FTD primarily affects frontal and temporal lobes, causing early personality, judgment, and language changes. Memory may remain preserved, highlighting selective network vulnerability.

Proteinopathies including tau, TDP-43, and FUS guide distinct symptom clusters. Impairments in social cognition often precede intellectual decline, underscoring the importance of early behavioral observation.

FTD shows that identity and behavior can erode even as core cognitive abilities remain intact.

References

Emerging & Overlooked Neurodegenerative Conditions

Rare and emerging conditions challenge conventional frameworks. Many share mechanisms with common dementias but are underrecognized. Neuroinflammation, mitochondrial dysfunction, and genetic modulation often drive these disorders.

Studying these conditions informs interventions across all neurodegenerative diseases and highlights mechanisms previously underestimated.

Rare conditions today may define tomorrow’s central strategies as detection and understanding evolve.