Wednesday, 14 August 2013


God brings men into deep waters not to drown them, but to cleanse them. Dementia lures men onto the horizon and detain their insight and dignity.
 A protein that accumulates in healthy aging brains could prove to be the culprit behind the natural forgetfulness that comes with growing old as well as advanced neurodegenerative diseases such as Alzheimer's, according to a new study.

A bend in the road is not the end of the road...unless you fail to make the turn.

The protein, known as C1q, accumulates on the brain's synapses as people age, potentially gumming up the works, according to the study.

A post-mortem review of mouse and human brains found that the amount of C1q in the brain increases as much as 300-fold with ageing.

Better to lose count while naming your blessings than to lose your blessings to counting your troubles.

By comparing brain tissue from mice of varying ages as well as postmortem samples from a 2 month old infant and an older person, the researchers found that the growing C1q deposits weren't randomly distributed along nerve cells.

Instead, they heavily concentrate at synapses (the junctions between nerve cells), where they could hamper the conduction of electrical and chemical signals in the brain.

With regards to the study,"Synapses are not being lost, meanwhile, the synapses aren't working so good with all that C1q stuck to them. It's detrimental."

But C1q is known to play an important part in the developing brain during childhood this function could lead the protein to attack the synapses if triggered. Such an attack could be the cause of Alzheimer's disease and other neurodegenerative disorders.

This hypothesis runs counter to prevailing theories about Alzheimer's, which have focused on the accumulation of amyloid plaques in the brain as a cause of the disease.

The difficulties of life are intended to make us better, not bitter.

In a normal developing brain, synapses are both created and destroyed, a process comparable to "pruning" the brain by preserving necessary synapses and eliminating the excess.

"What wasn't clear is what the molecular basis of the synapse pruning was," the study said. "It involves a normal immune protein that people didn't even realize was in the brain -- C1q."

C1q is capable of clinging to the surface of foreign bodies such as bacteria or to bits of dead or dying human cells. This initiates a molecular chain reaction known as the complement cascade. One by one, the system's other proteins glom on, coating the offending cell or piece of debris. This in turn draws the attention of omnivorous immune cells that gobble up the target.

The study, hypothesises that diseases such as Alzheimer's might develop if the C1q that has accumulated on the synapses triggers an immune system attack against them.

A gem cannot be polished without friction, nor a man perfected without trials.

The first regions of the brain to show a dramatic increase in C1q are places like the hippocampus and substantia nigra, the precise brain regions most vulnerable to neurodegenerative diseases like Alzheimer's and Parkinson's disease, respectively. Another region affected early on, the piriform cortex, is associated with the sense of smell, whose loss often heralds the onset of neurodegenerative disease.

If we will be quiet and ready enough, we shall find compensation in every disappointment.