Alzheimer's disease is the commonest dementia. One major characteristic of its pathology is accumulation of amyloid-beta (Abeta) as insoluble deposits in brain parenchyma and in blood vessel walls [cerebral amyloid angiopathy (CAA)]. The distribution of Abeta deposits in the basement membranes of cerebral capillaries and arteries corresponds to the perivascular drainage pathways by which interstitial fluid (ISF) and solutes are eliminated from the brain--effectively the lymphatic drainage of the brain. Theoretical models suggest that vessel pulsations supply the motive force for perivascular drainage of ISF and solutes. As arteries stiffen with age, the amplitude of pulsations is reduced and insoluble Abeta is deposited in ISF drainage pathways as CAA, thus, further impeding the drainage of soluble Abeta. Failure of perivascular drainage of Abeta and deposition of Abeta in the walls of arteries has two major consequences: (i) intracerebral hemorrhage associated with rupture of Abeta-laden arteries in CAA; and (ii) Alzheimer's disease in which failure of elimination of ISF, Abeta and other soluble metabolites from the brain alters homeostasis and the neuronal environment resulting in cognitive decline and dementia. Therapeutic strategies that improve elimination of Abeta and other soluble metabolites from the brain may prevent cognitive decline in Alzheimer's disease.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1750-3639.2008.00133.x

Perivascular drainage of amyloid-beta peptides from the brain and its failure in cerebral amyloid angiopathy and Alzheimer's disease.

This edition has been revised to include new data on genetics, molecular biology, and the role of cellular structures on one side and the growing experience with MR patterns of less common myelin disorders on the other. In addition, chapters have been added on disorders of which the white matter involvement was previously unclear.

Magnetic Resonance of Myelin, Myelination, and Myelin Disorders

There is firm physiological evidence for the lymphatic drainage of interstitial fluid and cerebrospinal fluid from the brains of rats, rabbits and cats. The object of this review, is to describe firstly the morphological aspects of lymphatic drainage pathways from the rat brain and secondly, to explore through scanning and transmission electron microscope techniques, the possibility of similar lymphatic drainage pathways in man.

Interstitial and oedema fluid spreads diffusely through the white matter in the rat and appears to drain into the ventricular cerebrospinal fluid. In grey matter, however, tracers pass along perivascular spaces to the surface of the brain and into the cerebrospinal fluid. Paravascular compartments in the subarachnoid space follow the course of major arterial branches to the circle of Willis and thence along the ethmoidal arteries to the cribriform plate of the ethmoid bone. Particulate tracers, such as Indian ink, enter channels in the arachnoid beneath the olfactory bulbs and connect directly with nasal lymphatics through channels which pass through holes in the cribriform plate. Proteins and other solutes may also drain along other cranial nerves. Thus, there is a bulk flow pathway for interstitial and cerebrospinal fluid from the rat brain into cervical lymphatics.

In man, it is probable that diffuse interstitial drainage of fluid from the white matter occurs in a similar way to that in the rat. Furthermore, the anatomical pathways exist by which bulk drainage of fluid could occur along perivascular spaces from the grey matter into perivascular spaces of the leptomeningeal arteries and thence into the cerebrospinal fluid (CSF). Compartmentalisation of the subarachnoid space may allow directional flow of CSF to occur. Thus, although the vast bulk of CSF in man drains through arachnoid villi and granulations, anatomical pathways exist by which selective flow for lymphatic drainage of brain interstitial fluid and inflammatory cells could occur. Physiological evidence for traffic along such pathways in man, however, is still sparse. It seems probable that any lymphatic drainage of CSF in man is overshadowed by the high volume passage of CSF through the arachnoid granulations and villi.

Pathways of fluid drainage from the brain--morphological aspects and immunological significance in rat and man.

Chronic hydrocephalus that begins in childhood and progresses only very gradually is sometimes called "arrested" hydrocephalus. Data suggest that this state eventually can become symptomatic and may be treatable by shunting. However, the pathological substrate of the disorder is not entirely understood. We studied chronic hydrocephalus in rats, 9 months after induction by kaolin injection into the cisterna magna, and in humans. In both circumstances, destruction of periventricular white matter structures was worst in those with the largest ventricles. Structures damaged include the corpus callosum, corticospinal tract, and fimbria/fornix projections from the hippocampus. Myelin turnover was increased. These changes were associated with deficits of motor and cognitive function. The cerebral cortex was largely spared. There appears to be a threshold of ventricle size beyond which functional changes manifest, but this undoubtedly is modified by factors such as age of onset and rate of enlargement. These data support the need for persistent follow-up of patients with chronic, apparently stable hydrocephalus. A slight increase in size of already enlarged ventricles might cause significant axonal damage.

Chronic hydrocephalus in rats and humans: White matter loss and behavior changes

In the context of spina bifida, hydrocephalus is usually caused by crowding of the posterior fossa with obstruction to cerebrospinal fluid flow from the forth ventricle, and less often by malformation of the cerebral aqueduct. Enlargement of the cerebral ventricles causes gradual destruction of periventricular white matter axons. Motor, sensory, visual, and memory systems may be disturbed through involvement of the long projection axons, periventricular structures including the corpus callosum, and the fimbria-fornix pathway. Secondary changes occur in neuronal cell bodies and synapses, but there is minimal death of neurons. The clinical syndrome of hydrocephalic brain dysfunction is thus due to subcortical disconnection. Some of the brain dysfunction is reversible by shunting, probably through restoration of cerebral blood flow and normalization of the extracellular environment. However, destroyed axons cannot be restored.

Neuropathology and structural changes in hydrocephalus.

Histological and ultrastructural changes with experimental hydrocephalus in adult rabbits

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Histological and ultrastructural changes with experimental hydrocephalus in adult rabbits