MODULE SUPPLEMENT: NEUROLOGICAL SYSTEM
Changes in Dendritic Processes

Dendrites bring information into the body (soma) of the neuron and are thus critical elements in the communication processes of the nervous system.

[See Unraveling the Mystery: Neurons and Their Jobs--Alzheimer's Disease Education & Referral Center for a picture of the neuron with its connections. NOTE: This link will open in a new browser window which you can close to return here.]

Although data are somewhat conflicting and may differ between what is found in animals and what is found in humans, there appears to be a decrease in dendritic density with loss of synapses. However, there are also data that suggest that, in humans, when neurons are lost the surviving neurons retain the capacity for "reactive synaptogenesis", or new dendritic growth and branching which can compensate for neuronal loss, although this may be slower in older than younger individuals (Cotman & Peterson, 1990).

Interestingly, studies done by Dr. Diamond and her colleagues at Berkeley have demonstrated that (in animals) it's possible to enhance the density of dendritic spines by exposing the animals to "enriched environments" - that is, environments with a lot of things to do and toys to play with.

[See Successful Aging of the Healthy Brain by Marian Diamond for background on Dr. Diamond's work and Do Brain Studies Point the Way to a 'Learning Vaccine'? for a discussion by Paul Naussbaum on research related to brain stimulation and healthy brain aging. NOTE: These links will open in new browser windows which you can close to return here.]

While this is positive, and suggests that small injuries may be repaired and that activity throughout the life span may help maintain dendritic connections, Agnati et al. (1991) pointed out that when neuronal depopulation occurs, those remaining may decrease the range of responses possible, even if they branch out and recreate connections with other neurons.

This effect will be seen later when changes that occur in muscle innervation are discussed. In addition, some neuropathologic features of Alzheimer's Disease may be interpreted as remnants of abortive compensatory responses.